https://wiki.oroboros.at/api.php?action=feedcontributions&user=Oroboros&feedformat=atomBioblast - User contributions [en]2024-03-29T09:35:59ZUser contributionsMediaWiki 1.36.1https://wiki.oroboros.at/index.php?title=Hickey_2012_J_Comp_Physiol_B&diff=44353Hickey 2012 J Comp Physiol B2013-03-24T18:48:38Z<p>Oroboros: </p>
<hr />
<div>{{Publication<br />
|title=Hickey AJ, Renshaw GM, Speers-Roesch B, Richards JG, Wang Y, Farrell AP, Brauner CJ (2012) A radical approach to beating hypoxia: depressed free radical release from heart fibres of the hypoxia-tolerant epaulette shark (''Hemiscyllum ocellatum''). J Comp Physiol B 182: 91-100.<br />
|info=[http://www.ncbi.nlm.nih.gov/pubmed/21748398 PMID:21748398]<br />
|authors=Hickey AJ, Renshaw GM, Speers-Roesch B, Richards JG, Wang Y, Farrell AP, Brauner CJ<br />
|year=2012<br />
|journal=J Comp Physiol B<br />
|abstract=Hypoxia and warm ischemia are primary concerns in ischemic heart disease and transplant and trauma. Hypoxia impacts tissue ATP supply and can induce mitochondrial dysfunction that elevates reactive species release. The epaulette shark, ''Hemiscyllum ocellatum'', is remarkably tolerant of severe hypoxia at temperatures up to 34 °C, and therefore provides a valuable model to study warm hypoxia tolerance. Mitochondrial function was tested in saponin permeabilised ventricle fibres using [[high-resolution respirometry]] coupled with purpose-built fluorospectrometers. Ventricular mitochondrial function, stability and reactive species production of the epaulette shark was compared with that of the hypoxia-sensitive shovelnose ray, ''Aptychotrema rostrata''. Fibres were prepared from each species acclimated to normoxic water conditions, or following a 2 h, acute hypoxic exposure at levels representing 40% of each species' critical oxygen tension. Although mitochondrial respiratory fluxes for normoxia-acclimated animals were similar for both species, reactive species production in the epaulette shark was approximately half that of the shovelnose ray under normoxic conditions, even when normalised to tissue oxidative phosphorylation flux. The hypoxia-sensitive shovelnose ray halved oxidative phosphorylation flux and cytochrome ''c'' oxidase flux was depressed by 34% following hypoxic stress. In contrast, oxidative phosphorylation flux of the epaulette shark ventricular fibres isolated from acute hypoxia exposed the animals remained similar to those from normoxia-acclimated animals. However, uncoupling of respiration revealed depressed electron transport systems in both species following hypoxia exposure. Overall, the epaulette shark ventricular mitochondria showed greater oxidative phosphorylation stability and lower reactive species outputs with hypoxic exposure, and this may protect cardiac bioenergetic function in hypoxic tropical waters.<br />
|keywords=mitochondria, hypoxia tolerance, shark<br />
|mipnetlab=NZ Auckland Hickey AJ, CA_Vancouver_Richards JG<br />
}}<br />
{{Labeling<br />
|instruments=Oxygraph-2k, Spectrofluorometry<br />
|injuries=Hypoxia, Ischemia-Reperfusion; Preservation, RONS; Oxidative Stress<br />
|tissues=Heart<br />
|preparations=Permeabilized tissue<br />
|couplingstates=OXPHOS<br />
}}<br />
==Product information==<br />
<br />
*[[O2k-Fluorescence LED2-Module]]</div>Oroboroshttps://wiki.oroboros.at/index.php?title=Bianchi_2004_J_Biol_Chem&diff=44352Bianchi 2004 J Biol Chem2013-03-24T18:43:23Z<p>Oroboros: </p>
<hr />
<div>{{Publication<br />
|title=Bianchi C, Genova ML, Parenti Castelli G, Lenaz G (2004) The mitochondrial respiratory chain is partially organized in a supercomplex assembly: kinetic evidence using flux control analysis. J Biol Chem 279: 36562-36569.<br />
|info=[http://www.ncbi.nlm.nih.gov/pubmed/15205457 PMID: 15205457 Open Access]<br />
|authors=Bianchi C, Genova ML, Parenti Castelli G, Lenaz G<br />
|year=2004<br />
|journal=J Biol Chem<br />
|abstract=The model of the respiratory chain in which the enzyme complexes are independently embedded in the lipid bilayer of the inner mitochondrial membrane and connected by randomly diffusing coenzyme Q and cytochrome c is mostly favored. However, multicomplex units can be isolated from mammalian mitochondria, suggesting a model based on direct electron channeling between complexes. Kinetic testing using metabolic flux control analysis can discriminate between the two models: the former model implies that each enzyme may be rate-controlling to a different extent, whereas in the latter, the whole metabolic pathway would behave as a single supercomplex and inhibition of any one of its components would elicit the same flux control. In particular, in the absence of other components of the oxidative phosphorylation apparatus (i.e. ATP synthase, membrane potential, carriers), the existence of a supercomplex would elicit a flux control coefficient near unity for each respiratory complex, and the sum of all coefficients would be well above unity. Using bovine heart mitochondria and submitochondrial particles devoid of substrate permeability barriers, we investigated the flux control coefficients of the complexes involved in aerobic NADH oxidation (I, III, IV) and in succinate oxidation (II, III, IV). Both Complexes I and III were found to be highly rate-controlling over NADH oxidation, a strong kinetic evidence suggesting the existence of functionally relevant association between the two complexes, whereas Complex IV appears randomly distributed. Moreover, we show that Complex II is fully rate-limiting for succinate oxidation, clearly indicating the absence of substrate channeling toward Complexes III and IV.<br />
|keywords=Supercomplex<br />
|discipline=Mitochondrial Physiology, Biomedicine<br />
}}<br />
{{Labeling<br />
|instruments=Oxygraph-2k<br />
|organism=Mammals<br />
|taxonomic group=Mammals<br />
|tissues=Heart<br />
|preparations=Isolated Mitochondria, SMP<br />
|additional=bovine<br />
|discipline=Mitochondrial Physiology, Biomedicine<br />
}}</div>Oroboroshttps://wiki.oroboros.at/index.php?title=Bianchi_2004_J_Biol_Chem&diff=44351Bianchi 2004 J Biol Chem2013-03-24T18:43:12Z<p>Oroboros: </p>
<hr />
<div>{{Publication<br />
|title=Bianchi C, Genova ML, Parenti Castelli G, Lenaz G (2004) The mitochondrial respiratory chain is partially organized in a supercomplex assembly: kinetic evidence using flux control analysis. J Biol Chem 279: 36562-36569.<br />
|info=[http://www.ncbi.nlm.nih.gov/pubmed/15205457 PMID: 15205457 Open Access]<br />
|authors=Bianchi C, Genova ML, Parenti Castelli G, Lenaz G<br />
|year=2004<br />
|journal=J Biol Chem<br />
|abstract=The model of the respiratory chain in which the enzyme complexes are independently embedded in the lipid bilayer of the inner mitochondrial membrane and connected by randomly diffusing coenzyme Q and cytochrome c is mostly favored. However, multicomplex units can be isolated from mammalian mitochondria, suggesting a model based on direct electron channeling between complexes. Kinetic testing using metabolic flux control analysis can discriminate between the two models: the former model implies that each enzyme may be rate-controlling to a different extent, whereas in the latter, the whole metabolic pathway would behave as a single supercomplex and inhibition of any one of its components would elicit the same flux control. In particular, in the absence of other components of the oxidative phosphorylation apparatus (i.e. ATP synthase, membrane potential, carriers), the existence of a supercomplex would elicit a flux control coefficient near unity for each respiratory complex, and the sum of all coefficients would be well above unity. Using bovine heart mitochondria and submitochondrial particles devoid of substrate permeability barriers, we investigated the flux control coefficients of the complexes involved in aerobic NADH oxidation (I, III, IV) and in succinate oxidation (II, III, IV). Both Complexes I and III were found to be highly rate-controlling over NADH oxidation, a strong kinetic evidence suggesting the existence of functionally relevant association between the two complexes, whereas Complex IV appears randomly distributed. Moreover, we show that Complex II is fully rate-limiting for succinate oxidation, clearly indicating the absence of substrate channeling toward Complexes III and IV.<br />
|keywords=Supercomplex<br />
|discipline=Mitochondrial Physiology, Biomedicine<br />
}}<br />
{{Labeling<br />
|instruments=Oxygraph-2k<br />
|organism=Mammals<br />
|tissues=Heart<br />
|preparations=Isolated Mitochondria, SMP<br />
|additional=bovine<br />
|discipline=Mitochondrial Physiology, Biomedicine<br />
}}</div>Oroboroshttps://wiki.oroboros.at/index.php?title=Kiebish_2013_J_Lipid_Res&diff=44350Kiebish 2013 J Lipid Res2013-03-24T18:36:48Z<p>Oroboros: </p>
<hr />
<div>{{Publication<br />
|title=Kiebish MA, Yang K, Liu X, Mancuso DJ, Guan S, Zhao Z, Sims HF, Cerqua R, Cade WT, Han X, Gross RW (2013) Dysfunctional cardiac mitochondrial bioenergetic, lipidomic, and signaling in a murine model of Barth syndrome. J Lipid Res [Epub ahead of print].<br />
|info=[http://www.ncbi.nlm.nih.gov/pubmed/23410936 PMID: 23410936 Open Access]<br />
|authors=Kiebish MA, Yang K, Liu X, Mancuso DJ, Guan S, Zhao Z, Sims HF, Cerqua R, Cade WT, Han X, Gross RW<br />
|year=2013<br />
|journal=J Lipid Res<br />
|abstract=Barth syndrome is a complex metabolic disorder caused by mutations in the mitochondrial transacylase Tafazzin. Recently, an inducible Tafazzin shRNA knockdown mouse model was generated to deconvolute the complex bioenergetic phenotype of this disease. To investigate the underlying cause of hemodynamic dysfunction in Barth syndrome, we interrogated the cardiac structural and signaling lipidome of this mouse model as well as its myocardial bioenergetic phenotype. A decrease in the distribution of cardiolipin molecular species and robust increases in monolysocardiolipin and dilysocardiolipin were demonstrated. Additionally, the contents of choline and ethanolamine glycerophospholipid molecular species containing precursors for lipid signaling at the sn-2 position were altered. Lipidomic analyses revealed specific dysregulation of HETEs, prostanoids, as well as oxidized linoleic and docosahexaenoic metabolites. Bioenergetic interrogation uncovered differential substrate utilization as well as deceases in Complex III and V activities. Transgenic expression of cardiolipin synthase or iPLA2γ ablation in Tafazzin deficient mice did not rescue the observed phenotype. These results underscore the complex nature of alterations in cardiolipin metabolism mediated by Tafazzin loss of function. Collectively, we identified specific lipidomic, bioenergetic and signaling alterations in a murine model that parallel those of Barth syndrome thereby providing novel insights into the pathophysiology of this debilitating disease.<br />
|keywords=Lipidome; Cardiolipin; Tafazzin; Phospholipase; Cardiolipin synthase; Electron transport chain<br />
|mipnetlab=US MO St Louis Gross RW,<br />
}}<br />
{{Labeling<br />
|instruments=Oxygraph-2k<br />
|injuries=Mitochondrial Disease; Degenerative Disease and Defect, Genetic Defect; Knockdown; Overexpression<br />
|organism=Mouse<br />
|tissues=Heart<br />
|preparations=Isolated Mitochondria<br />
|enzymes=Complex III, Complex V; ATP Synthase<br />
}}</div>Oroboroshttps://wiki.oroboros.at/index.php?title=Kiebish_2013_J_Lipid_Res&diff=44349Kiebish 2013 J Lipid Res2013-03-24T18:36:17Z<p>Oroboros: </p>
<hr />
<div>{{Publication<br />
|title=Kiebish MA, Yang K, Liu X, Mancuso DJ, Guan S, Zhao Z, Sims HF, Cerqua R, Cade WT, Han X, Gross RW (2013) Dysfunctional cardiac mitochondrial bioenergetic, lipidomic, and signaling in a murine model of Barth syndrome. J Lipid Res [Epub ahead of print].<br />
|info=[http://www.ncbi.nlm.nih.gov/pubmed/23410936 PMID: 23410936 Open Access]<br />
|authors=Kiebish MA, Yang K, Liu X, Mancuso DJ, Guan S, Zhao Z, Sims HF, Cerqua R, Cade WT, Han X, Gross RW<br />
|year=2013<br />
|journal=J Lipid Res<br />
|abstract=Barth syndrome is a complex metabolic disorder caused by mutations in the mitochondrial transacylase Tafazzin. Recently, an inducible Tafazzin shRNA knockdown mouse model was generated to deconvolute the complex bioenergetic phenotype of this disease. To investigate the underlying cause of hemodynamic dysfunction in Barth syndrome, we interrogated the cardiac structural and signaling lipidome of this mouse model as well as its myocardial bioenergetic phenotype. A decrease in the distribution of cardiolipin molecular species and robust increases in monolysocardiolipin and dilysocardiolipin were demonstrated. Additionally, the contents of choline and ethanolamine glycerophospholipid molecular species containing precursors for lipid signaling at the sn-2 position were altered. Lipidomic analyses revealed specific dysregulation of HETEs, prostanoids, as well as oxidized linoleic and docosahexaenoic metabolites. Bioenergetic interrogation uncovered differential substrate utilization as well as deceases in Complex III and V activities. Transgenic expression of cardiolipin synthase or iPLA2γ ablation in Tafazzin deficient mice did not rescue the observed phenotype. These results underscore the complex nature of alterations in cardiolipin metabolism mediated by Tafazzin loss of function. Collectively, we identified specific lipidomic, bioenergetic and signaling alterations in a murine model that parallel those of Barth syndrome thereby providing novel insights into the pathophysiology of this debilitating disease.<br />
|keywords=Lipidome; Cardiolipin; Tafazzin; Phospholipase; Cardiolipin synthase; Electron transport chain<br />
|mipnetlab=US MO St Louis Gross RW,<br />
}}<br />
{{Labeling<br />
|instruments=Oxygraph-2k<br />
|injuries=Mitochondrial Disease; Degenerative Disease and Defect, Genetic Defect; Knockdown; Overexpression<br />
|organism=Mouse<br />
|taxonomic group=Mammals, Other invertebrates<br />
|tissues=Heart<br />
|preparations=Isolated Mitochondria<br />
|enzymes=Complex III, Complex V; ATP Synthase<br />
}}</div>Oroboroshttps://wiki.oroboros.at/index.php?title=Kiebish_2013_J_Lipid_Res&diff=44348Kiebish 2013 J Lipid Res2013-03-24T18:35:44Z<p>Oroboros: </p>
<hr />
<div>{{Publication<br />
|title=Kiebish MA, Yang K, Liu X, Mancuso DJ, Guan S, Zhao Z, Sims HF, Cerqua R, Cade WT, Han X, Gross RW (2013) Dysfunctional cardiac mitochondrial bioenergetic, lipidomic, and signaling in a murine model of Barth syndrome. J Lipid Res [Epub ahead of print].<br />
|info=[http://www.ncbi.nlm.nih.gov/pubmed/23410936 PMID: 23410936 Open Access]<br />
|authors=Kiebish MA, Yang K, Liu X, Mancuso DJ, Guan S, Zhao Z, Sims HF, Cerqua R, Cade WT, Han X, Gross RW<br />
|year=2013<br />
|journal=J Lipid Res<br />
|abstract=Barth syndrome is a complex metabolic disorder caused by mutations in the mitochondrial transacylase Tafazzin. Recently, an inducible Tafazzin shRNA knockdown mouse model was generated to deconvolute the complex bioenergetic phenotype of this disease. To investigate the underlying cause of hemodynamic dysfunction in Barth syndrome, we interrogated the cardiac structural and signaling lipidome of this mouse model as well as its myocardial bioenergetic phenotype. A decrease in the distribution of cardiolipin molecular species and robust increases in monolysocardiolipin and dilysocardiolipin were demonstrated. Additionally, the contents of choline and ethanolamine glycerophospholipid molecular species containing precursors for lipid signaling at the sn-2 position were altered. Lipidomic analyses revealed specific dysregulation of HETEs, prostanoids, as well as oxidized linoleic and docosahexaenoic metabolites. Bioenergetic interrogation uncovered differential substrate utilization as well as deceases in Complex III and V activities. Transgenic expression of cardiolipin synthase or iPLA2γ ablation in Tafazzin deficient mice did not rescue the observed phenotype. These results underscore the complex nature of alterations in cardiolipin metabolism mediated by Tafazzin loss of function. Collectively, we identified specific lipidomic, bioenergetic and signaling alterations in a murine model that parallel those of Barth syndrome thereby providing novel insights into the pathophysiology of this debilitating disease.<br />
|keywords=Lipidome; Cardiolipin; Tafazzin; Phospholipase; Cardiolipin synthase; Electron transport chain<br />
|mipnetlab=US MO St Louis Gross RW,<br />
}}<br />
{{Labeling<br />
|instruments=Oxygraph-2k<br />
|injuries=Mitochondrial Disease; Degenerative Disease and Defect, Genetic Defect; Knockdown; Overexpression<br />
|organism=Mouse<br />
|tissues=Heart<br />
|preparations=Isolated Mitochondria<br />
|enzymes=Complex III, Complex V; ATP Synthase<br />
}}</div>Oroboroshttps://wiki.oroboros.at/index.php?title=Template:Labeling&diff=44347Template:Labeling2013-03-24T18:33:33Z<p>Oroboros: </p>
<hr />
<div><noinclude><br />
This is the "labeling" template.<br />
It should be called in the following format:<br />
<pre><br />
{{labeling<br />
|high-resolution respirometry=<br />
|injuries=<br />
|diseases=<br />
|organism=<br />
|taxonomic group=<br />
|tissues=<br />
|model cell lines=<br />
|preparations=<br />
|couplingstates=<br />
|substratestates<br />
|enzymes=<br />
|kinetics=<br />
|topics=<br />
|editor=<br />
|additional=<br />
}}<br />
</pre><br />
Edit the page to see the template text.<br />
</noinclude><includeonly><br />
'''Labels:'''<br />
{{#if: {{{instruments|}}} |'''High-Resolution Respirometry:''' {{#arraymap:{{{instruments|}}}|,|x|[[Instrument and method::x]]}}&nbsp;}}{{#if: {{{injuries|}}} |'''Injuries and Adaptations:''' {{#arraymap:{{{injuries|}}}|,|x|[[Injury and adaptation::x]]}}&nbsp;}}{{#if: {{{diseases|}}} |'''Diseases:''' {{#arraymap:{{{diseases|}}}|,|x|[[Diseases::x]]}}&nbsp;}}{{#if: {{{organism|}}} |'''Organism:''' {{#arraymap:{{{organism|}}}|,|x|[[Organism::x]]}}&nbsp;}}{{#if: {{{taxonomic group|}}} |'''Taxonomic group:''' {{#arraymap:{{{taxonomic group|}}}|,|@@|[[Taxonomic group::@@]]}}&nbsp;}}{{#if: {{{tissues|}}} |'''Tissues and Cells:''' {{#arraymap:{{{tissues|}}}|,|x|[[Tissue and cell type::x]]}}&nbsp;}}{{#if: {{{model cell lines|}}} |'''Model cell lines:''' {{#arraymap:{{{model cell lines|}}}|,|x|[[Model cell lines::x]]}}&nbsp;}}{{#if: {{{preparations|}}} |'''Preparations:''' {{#arraymap:{{{preparations|}}}|,|x|[[Preparation::x]]}}&nbsp;}}{{#if: {{{couplingstates|}}} |'''Coupling states:''' {{#arraymap:{{{couplingstates|}}}|,|x|[[Coupling states::x]]}}&nbsp;}}{{#if: {{{substratestates|}}} |'''Substrate states:''' {{#arraymap:{{{substratestates|}}}|,|x|[[Substrate states::x]]}}&nbsp;}}{{#if: {{{enzymes|}}} |'''Enzymes:''' {{#arraymap:{{{enzymes|}}}|,|x|[[Enzyme::x]]}}&nbsp;}}{{#if: {{{kinetics|}}} |'''Kinetics:''' {{#arraymap:{{{kinetics|}}}|,|x|[[Kinetic::x]]}}&nbsp;}}{{#if: {{{topics|}}} |'''Topics:''' {{#arraymap:{{{topics|}}}|,|x|[[Topic::x]]}}&nbsp;}}{{#if: {{{editor|}}} |'''Editor:''' {{#arraymap:{{{editor|}}}|,|x|[[Editor::x]]}}&nbsp;}}{{#if: {{{additional|}}} |'''Additional topics:''' {{#arraymap:{{{additional|}}}|,|x|[[additional label::x]]}}&nbsp;}}<br />
</includeonly></div>Oroboroshttps://wiki.oroboros.at/index.php?title=Kiebish_2013_J_Lipid_Res&diff=44346Kiebish 2013 J Lipid Res2013-03-24T18:32:05Z<p>Oroboros: </p>
<hr />
<div>{{Publication<br />
|title=Kiebish MA, Yang K, Liu X, Mancuso DJ, Guan S, Zhao Z, Sims HF, Cerqua R, Cade WT, Han X, Gross RW (2013) Dysfunctional cardiac mitochondrial bioenergetic, lipidomic, and signaling in a murine model of Barth syndrome. J Lipid Res [Epub ahead of print].<br />
|info=[http://www.ncbi.nlm.nih.gov/pubmed/23410936 PMID: 23410936 Open Access]<br />
|authors=Kiebish MA, Yang K, Liu X, Mancuso DJ, Guan S, Zhao Z, Sims HF, Cerqua R, Cade WT, Han X, Gross RW<br />
|year=2013<br />
|journal=J Lipid Res<br />
|abstract=Barth syndrome is a complex metabolic disorder caused by mutations in the mitochondrial transacylase Tafazzin. Recently, an inducible Tafazzin shRNA knockdown mouse model was generated to deconvolute the complex bioenergetic phenotype of this disease. To investigate the underlying cause of hemodynamic dysfunction in Barth syndrome, we interrogated the cardiac structural and signaling lipidome of this mouse model as well as its myocardial bioenergetic phenotype. A decrease in the distribution of cardiolipin molecular species and robust increases in monolysocardiolipin and dilysocardiolipin were demonstrated. Additionally, the contents of choline and ethanolamine glycerophospholipid molecular species containing precursors for lipid signaling at the sn-2 position were altered. Lipidomic analyses revealed specific dysregulation of HETEs, prostanoids, as well as oxidized linoleic and docosahexaenoic metabolites. Bioenergetic interrogation uncovered differential substrate utilization as well as deceases in Complex III and V activities. Transgenic expression of cardiolipin synthase or iPLA2γ ablation in Tafazzin deficient mice did not rescue the observed phenotype. These results underscore the complex nature of alterations in cardiolipin metabolism mediated by Tafazzin loss of function. Collectively, we identified specific lipidomic, bioenergetic and signaling alterations in a murine model that parallel those of Barth syndrome thereby providing novel insights into the pathophysiology of this debilitating disease.<br />
|keywords=Lipidome; Cardiolipin; Tafazzin; Phospholipase; Cardiolipin synthase; Electron transport chain<br />
|mipnetlab=US MO St Louis Gross RW,<br />
}}<br />
{{Labeling<br />
|instruments=Oxygraph-2k<br />
|injuries=Mitochondrial Disease; Degenerative Disease and Defect, Genetic Defect; Knockdown; Overexpression<br />
|organism=Mouse<br />
|taxonomic group=Mammals, Birds, Reptiles, Chelicerates, Myriapods, Annelids, Molluscs, Nematodes, Platyhelminthes, Cnidaria and Porifera, Other invertebrates, Fungi, Plants, Protists, Eubacteria, Archea<br />
|tissues=Heart<br />
|preparations=Isolated Mitochondria<br />
|enzymes=Complex III, Complex V; ATP Synthase<br />
}}</div>Oroboroshttps://wiki.oroboros.at/index.php?title=Kiebish_2013_J_Lipid_Res&diff=44345Kiebish 2013 J Lipid Res2013-03-24T18:31:19Z<p>Oroboros: </p>
<hr />
<div>{{Publication<br />
|title=Kiebish MA, Yang K, Liu X, Mancuso DJ, Guan S, Zhao Z, Sims HF, Cerqua R, Cade WT, Han X, Gross RW (2013) Dysfunctional cardiac mitochondrial bioenergetic, lipidomic, and signaling in a murine model of Barth syndrome. J Lipid Res [Epub ahead of print].<br />
|info=[http://www.ncbi.nlm.nih.gov/pubmed/23410936 PMID: 23410936 Open Access]<br />
|authors=Kiebish MA, Yang K, Liu X, Mancuso DJ, Guan S, Zhao Z, Sims HF, Cerqua R, Cade WT, Han X, Gross RW<br />
|year=2013<br />
|journal=J Lipid Res<br />
|abstract=Barth syndrome is a complex metabolic disorder caused by mutations in the mitochondrial transacylase Tafazzin. Recently, an inducible Tafazzin shRNA knockdown mouse model was generated to deconvolute the complex bioenergetic phenotype of this disease. To investigate the underlying cause of hemodynamic dysfunction in Barth syndrome, we interrogated the cardiac structural and signaling lipidome of this mouse model as well as its myocardial bioenergetic phenotype. A decrease in the distribution of cardiolipin molecular species and robust increases in monolysocardiolipin and dilysocardiolipin were demonstrated. Additionally, the contents of choline and ethanolamine glycerophospholipid molecular species containing precursors for lipid signaling at the sn-2 position were altered. Lipidomic analyses revealed specific dysregulation of HETEs, prostanoids, as well as oxidized linoleic and docosahexaenoic metabolites. Bioenergetic interrogation uncovered differential substrate utilization as well as deceases in Complex III and V activities. Transgenic expression of cardiolipin synthase or iPLA2γ ablation in Tafazzin deficient mice did not rescue the observed phenotype. These results underscore the complex nature of alterations in cardiolipin metabolism mediated by Tafazzin loss of function. Collectively, we identified specific lipidomic, bioenergetic and signaling alterations in a murine model that parallel those of Barth syndrome thereby providing novel insights into the pathophysiology of this debilitating disease.<br />
|keywords=Lipidome; Cardiolipin; Tafazzin; Phospholipase; Cardiolipin synthase; Electron transport chain<br />
|mipnetlab=US MO St Louis Gross RW,<br />
}}<br />
{{Labeling<br />
|instruments=Oxygraph-2k<br />
|injuries=Mitochondrial Disease; Degenerative Disease and Defect, Genetic Defect; Knockdown; Overexpression<br />
|organism=Mouse<br />
|taxonomic group=Mammals, Reptiles, Chelicerates, Myriapods, Annelids, Molluscs, Nematodes, Platyhelminthes, Cnidaria and Porifera, Other invertebrates, Fungi, Plants, Protists, Eubacteria, Archea<br />
|tissues=Heart<br />
|preparations=Isolated Mitochondria<br />
|enzymes=Complex III, Complex V; ATP Synthase<br />
}}</div>Oroboroshttps://wiki.oroboros.at/index.php?title=Kiebish_2013_J_Lipid_Res&diff=44344Kiebish 2013 J Lipid Res2013-03-24T18:21:35Z<p>Oroboros: </p>
<hr />
<div>{{Publication<br />
|title=Kiebish MA, Yang K, Liu X, Mancuso DJ, Guan S, Zhao Z, Sims HF, Cerqua R, Cade WT, Han X, Gross RW (2013) Dysfunctional cardiac mitochondrial bioenergetic, lipidomic, and signaling in a murine model of Barth syndrome. J Lipid Res [Epub ahead of print].<br />
|info=[http://www.ncbi.nlm.nih.gov/pubmed/23410936 PMID: 23410936 Open Access]<br />
|authors=Kiebish MA, Yang K, Liu X, Mancuso DJ, Guan S, Zhao Z, Sims HF, Cerqua R, Cade WT, Han X, Gross RW<br />
|year=2013<br />
|journal=J Lipid Res<br />
|abstract=Barth syndrome is a complex metabolic disorder caused by mutations in the mitochondrial transacylase Tafazzin. Recently, an inducible Tafazzin shRNA knockdown mouse model was generated to deconvolute the complex bioenergetic phenotype of this disease. To investigate the underlying cause of hemodynamic dysfunction in Barth syndrome, we interrogated the cardiac structural and signaling lipidome of this mouse model as well as its myocardial bioenergetic phenotype. A decrease in the distribution of cardiolipin molecular species and robust increases in monolysocardiolipin and dilysocardiolipin were demonstrated. Additionally, the contents of choline and ethanolamine glycerophospholipid molecular species containing precursors for lipid signaling at the sn-2 position were altered. Lipidomic analyses revealed specific dysregulation of HETEs, prostanoids, as well as oxidized linoleic and docosahexaenoic metabolites. Bioenergetic interrogation uncovered differential substrate utilization as well as deceases in Complex III and V activities. Transgenic expression of cardiolipin synthase or iPLA2γ ablation in Tafazzin deficient mice did not rescue the observed phenotype. These results underscore the complex nature of alterations in cardiolipin metabolism mediated by Tafazzin loss of function. Collectively, we identified specific lipidomic, bioenergetic and signaling alterations in a murine model that parallel those of Barth syndrome thereby providing novel insights into the pathophysiology of this debilitating disease.<br />
|keywords=Lipidome; Cardiolipin; Tafazzin; Phospholipase; Cardiolipin synthase; Electron transport chain<br />
|mipnetlab=US MO St Louis Gross RW,<br />
}}<br />
{{Labeling<br />
|instruments=Oxygraph-2k<br />
|injuries=Mitochondrial Disease; Degenerative Disease and Defect, Genetic Defect; Knockdown; Overexpression<br />
|organism=Mouse<br />
|taxonomic group=Mammals, Birds, Reptiles, Chelicerates, Myriapods, Annelids, Molluscs, Nematodes, Platyhelminthes, Cnidaria and Porifera, Other invertebrates, Fungi, Plants, Protists, Eubacteria, Archea<br />
|tissues=Heart<br />
|preparations=Isolated Mitochondria<br />
|enzymes=Complex III, Complex V; ATP Synthase<br />
}}</div>Oroboroshttps://wiki.oroboros.at/index.php?title=Kiebish_2013_J_Lipid_Res&diff=44343Kiebish 2013 J Lipid Res2013-03-24T11:45:51Z<p>Oroboros: </p>
<hr />
<div>{{Publication<br />
|title=Kiebish MA, Yang K, Liu X, Mancuso DJ, Guan S, Zhao Z, Sims HF, Cerqua R, Cade WT, Han X, Gross RW (2013) Dysfunctional cardiac mitochondrial bioenergetic, lipidomic, and signaling in a murine model of Barth syndrome. J Lipid Res [Epub ahead of print].<br />
|info=[http://www.ncbi.nlm.nih.gov/pubmed/23410936 PMID: 23410936 Open Access]<br />
|authors=Kiebish MA, Yang K, Liu X, Mancuso DJ, Guan S, Zhao Z, Sims HF, Cerqua R, Cade WT, Han X, Gross RW<br />
|year=2013<br />
|journal=J Lipid Res<br />
|abstract=Barth syndrome is a complex metabolic disorder caused by mutations in the mitochondrial transacylase Tafazzin. Recently, an inducible Tafazzin shRNA knockdown mouse model was generated to deconvolute the complex bioenergetic phenotype of this disease. To investigate the underlying cause of hemodynamic dysfunction in Barth syndrome, we interrogated the cardiac structural and signaling lipidome of this mouse model as well as its myocardial bioenergetic phenotype. A decrease in the distribution of cardiolipin molecular species and robust increases in monolysocardiolipin and dilysocardiolipin were demonstrated. Additionally, the contents of choline and ethanolamine glycerophospholipid molecular species containing precursors for lipid signaling at the sn-2 position were altered. Lipidomic analyses revealed specific dysregulation of HETEs, prostanoids, as well as oxidized linoleic and docosahexaenoic metabolites. Bioenergetic interrogation uncovered differential substrate utilization as well as deceases in Complex III and V activities. Transgenic expression of cardiolipin synthase or iPLA2γ ablation in Tafazzin deficient mice did not rescue the observed phenotype. These results underscore the complex nature of alterations in cardiolipin metabolism mediated by Tafazzin loss of function. Collectively, we identified specific lipidomic, bioenergetic and signaling alterations in a murine model that parallel those of Barth syndrome thereby providing novel insights into the pathophysiology of this debilitating disease.<br />
|keywords=Lipidome; Cardiolipin; Tafazzin; Phospholipase; Cardiolipin synthase; Electron transport chain<br />
|mipnetlab=US MO St Louis Gross RW,<br />
}}<br />
{{Labeling<br />
|instruments=Oxygraph-2k<br />
|injuries=Mitochondrial Disease; Degenerative Disease and Defect, Genetic Defect; Knockdown; Overexpression<br />
|organism=Mouse<br />
|tissues=Heart<br />
|preparations=Isolated Mitochondria<br />
|enzymes=Complex III, Complex V; ATP Synthase<br />
}}</div>Oroboroshttps://wiki.oroboros.at/index.php?title=Kiebish_2013_J_Lipid_Res&diff=44342Kiebish 2013 J Lipid Res2013-03-24T11:44:01Z<p>Oroboros: </p>
<hr />
<div>{{Publication<br />
|title=Kiebish MA, Yang K, Liu X, Mancuso DJ, Guan S, Zhao Z, Sims HF, Cerqua R, Cade WT, Han X, Gross RW (2013) Dysfunctional cardiac mitochondrial bioenergetic, lipidomic, and signaling in a murine model of Barth syndrome. J Lipid Res [Epub ahead of print].<br />
|info=[http://www.ncbi.nlm.nih.gov/pubmed/23410936 PMID: 23410936 Open Access]<br />
|authors=Kiebish MA, Yang K, Liu X, Mancuso DJ, Guan S, Zhao Z, Sims HF, Cerqua R, Cade WT, Han X, Gross RW<br />
|year=2013<br />
|journal=J Lipid Res<br />
|abstract=Barth syndrome is a complex metabolic disorder caused by mutations in the mitochondrial transacylase Tafazzin. Recently, an inducible Tafazzin shRNA knockdown mouse model was generated to deconvolute the complex bioenergetic phenotype of this disease. To investigate the underlying cause of hemodynamic dysfunction in Barth syndrome, we interrogated the cardiac structural and signaling lipidome of this mouse model as well as its myocardial bioenergetic phenotype. A decrease in the distribution of cardiolipin molecular species and robust increases in monolysocardiolipin and dilysocardiolipin were demonstrated. Additionally, the contents of choline and ethanolamine glycerophospholipid molecular species containing precursors for lipid signaling at the sn-2 position were altered. Lipidomic analyses revealed specific dysregulation of HETEs, prostanoids, as well as oxidized linoleic and docosahexaenoic metabolites. Bioenergetic interrogation uncovered differential substrate utilization as well as deceases in Complex III and V activities. Transgenic expression of cardiolipin synthase or iPLA2γ ablation in Tafazzin deficient mice did not rescue the observed phenotype. These results underscore the complex nature of alterations in cardiolipin metabolism mediated by Tafazzin loss of function. Collectively, we identified specific lipidomic, bioenergetic and signaling alterations in a murine model that parallel those of Barth syndrome thereby providing novel insights into the pathophysiology of this debilitating disease.<br />
|keywords=Lipidome; Cardiolipin; Tafazzin; Phospholipase; Cardiolipin synthase; Electron transport chain<br />
|mipnetlab=US MO St Louis Gross RW,<br />
}}<br />
{{Labeling<br />
|instruments=Oxygraph-2k<br />
|injuries=Mitochondrial Disease; Degenerative Disease and Defect, Genetic Defect; Knockdown; Overexpression<br />
|organism=Mouse, Mammals<br />
|taxonomic group=Mammals, Birds, Reptiles<br />
|tissues=Heart<br />
|preparations=Isolated Mitochondria<br />
|enzymes=Complex III, Complex V; ATP Synthase<br />
}}</div>Oroboroshttps://wiki.oroboros.at/index.php?title=Kiebish_2013_J_Lipid_Res&diff=44341Kiebish 2013 J Lipid Res2013-03-24T11:30:20Z<p>Oroboros: </p>
<hr />
<div>{{Publication<br />
|title=Kiebish MA, Yang K, Liu X, Mancuso DJ, Guan S, Zhao Z, Sims HF, Cerqua R, Cade WT, Han X, Gross RW (2013) Dysfunctional cardiac mitochondrial bioenergetic, lipidomic, and signaling in a murine model of Barth syndrome. J Lipid Res [Epub ahead of print].<br />
|info=[http://www.ncbi.nlm.nih.gov/pubmed/23410936 PMID: 23410936 Open Access]<br />
|authors=Kiebish MA, Yang K, Liu X, Mancuso DJ, Guan S, Zhao Z, Sims HF, Cerqua R, Cade WT, Han X, Gross RW<br />
|year=2013<br />
|journal=J Lipid Res<br />
|abstract=Barth syndrome is a complex metabolic disorder caused by mutations in the mitochondrial transacylase Tafazzin. Recently, an inducible Tafazzin shRNA knockdown mouse model was generated to deconvolute the complex bioenergetic phenotype of this disease. To investigate the underlying cause of hemodynamic dysfunction in Barth syndrome, we interrogated the cardiac structural and signaling lipidome of this mouse model as well as its myocardial bioenergetic phenotype. A decrease in the distribution of cardiolipin molecular species and robust increases in monolysocardiolipin and dilysocardiolipin were demonstrated. Additionally, the contents of choline and ethanolamine glycerophospholipid molecular species containing precursors for lipid signaling at the sn-2 position were altered. Lipidomic analyses revealed specific dysregulation of HETEs, prostanoids, as well as oxidized linoleic and docosahexaenoic metabolites. Bioenergetic interrogation uncovered differential substrate utilization as well as deceases in Complex III and V activities. Transgenic expression of cardiolipin synthase or iPLA2γ ablation in Tafazzin deficient mice did not rescue the observed phenotype. These results underscore the complex nature of alterations in cardiolipin metabolism mediated by Tafazzin loss of function. Collectively, we identified specific lipidomic, bioenergetic and signaling alterations in a murine model that parallel those of Barth syndrome thereby providing novel insights into the pathophysiology of this debilitating disease.<br />
|keywords=Lipidome; Cardiolipin; Tafazzin; Phospholipase; Cardiolipin synthase; Electron transport chain<br />
|mipnetlab=US MO St Louis Gross RW,<br />
}}<br />
{{Labeling<br />
|instruments=Oxygraph-2k<br />
|injuries=Mitochondrial Disease; Degenerative Disease and Defect, Genetic Defect; Knockdown; Overexpression<br />
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|preparations=Isolated Mitochondria<br />
|enzymes=Complex III, Complex V; ATP Synthase<br />
}}</div>Oroboroshttps://wiki.oroboros.at/index.php?title=Kiebish_2013_J_Lipid_Res&diff=44340Kiebish 2013 J Lipid Res2013-03-24T10:50:29Z<p>Oroboros: </p>
<hr />
<div>{{Publication<br />
|title=Kiebish MA, Yang K, Liu X, Mancuso DJ, Guan S, Zhao Z, Sims HF, Cerqua R, Cade WT, Han X, Gross RW (2013) Dysfunctional cardiac mitochondrial bioenergetic, lipidomic, and signaling in a murine model of Barth syndrome. J Lipid Res [Epub ahead of print].<br />
|info=[http://www.ncbi.nlm.nih.gov/pubmed/23410936 PMID: 23410936 Open Access]<br />
|authors=Kiebish MA, Yang K, Liu X, Mancuso DJ, Guan S, Zhao Z, Sims HF, Cerqua R, Cade WT, Han X, Gross RW<br />
|year=2013<br />
|journal=J Lipid Res<br />
|abstract=Barth syndrome is a complex metabolic disorder caused by mutations in the mitochondrial transacylase Tafazzin. Recently, an inducible Tafazzin shRNA knockdown mouse model was generated to deconvolute the complex bioenergetic phenotype of this disease. To investigate the underlying cause of hemodynamic dysfunction in Barth syndrome, we interrogated the cardiac structural and signaling lipidome of this mouse model as well as its myocardial bioenergetic phenotype. A decrease in the distribution of cardiolipin molecular species and robust increases in monolysocardiolipin and dilysocardiolipin were demonstrated. Additionally, the contents of choline and ethanolamine glycerophospholipid molecular species containing precursors for lipid signaling at the sn-2 position were altered. Lipidomic analyses revealed specific dysregulation of HETEs, prostanoids, as well as oxidized linoleic and docosahexaenoic metabolites. Bioenergetic interrogation uncovered differential substrate utilization as well as deceases in Complex III and V activities. Transgenic expression of cardiolipin synthase or iPLA2γ ablation in Tafazzin deficient mice did not rescue the observed phenotype. These results underscore the complex nature of alterations in cardiolipin metabolism mediated by Tafazzin loss of function. Collectively, we identified specific lipidomic, bioenergetic and signaling alterations in a murine model that parallel those of Barth syndrome thereby providing novel insights into the pathophysiology of this debilitating disease.<br />
|keywords=Lipidome; Cardiolipin; Tafazzin; Phospholipase; Cardiolipin synthase; Electron transport chain<br />
|mipnetlab=US MO St Louis Gross RW,<br />
}}<br />
{{Labeling<br />
|instruments=Oxygraph-2k<br />
|injuries=Mitochondrial Disease; Degenerative Disease and Defect, Genetic Defect; Knockdown; Overexpression<br />
|organism=Mouse<br />
|taxonomic group=Mammals, Birds, Fungi<br />
|tissues=Heart<br />
|preparations=Isolated Mitochondria<br />
|enzymes=Complex III, Complex V; ATP Synthase<br />
}}</div>Oroboroshttps://wiki.oroboros.at/index.php?title=Template:Abstract&diff=35499Template:Abstract2012-11-04T20:01:19Z<p>Oroboros: </p>
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== '''O2k-Catalogue OROBOROS - a guided tour to the O2k''' ==<br />
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::*'''[[O2k-Catalogue: Contents and concept]]''' <br />
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Product ID '''1'''#### '''[[Oxygraph-2k]]''' - the modular system for high-resolution respirometry. <br />
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::* '''>>> [[O2k-Catalogue: Complete OROBOROS Product List]]: including former series and all spares''' / Order information: [http://www.oroboros.at/?Purchase @OROBOROS]<br />
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== '''O2k-Catalogue OROBOROS''' - all products in current series ==<br />
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{{#ask: mainlabel=Title|[[Category:OroboroPedia]] | [[Product type::O2k]] <br />
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<hr />
<div>{{MitoPedia<br />
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|description='''LEAK respiration''' or LEAK oxygen flux, compensating for proton leak, slip and cation cycling, is measured as mitochondrial respiration in state ''L'', in the presence of reducing substrate(s), but absence of inorganic phosphate or ADP, or after inhibition of the [[phosphorylation system]]. In this non-phosphorylating resting state, the electrochemical proton gradient is increased to a maximum, exerting feedback control by depressing oxygen flux to a level determined by the [[proton leak]] and the H<sup>+</sup>/O ratio. In this state of maximum protonmotive force, LEAK respiration is higher than the LEAK component in state ''P'' ([[OXPHOS capacity]]).<br />
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<div>{{Publication<br />
|title=Armstrong C. and Staples J.F. 2010. The role of succinate dehydrogenase and oxaloacetate in mitochondrial metabolism during mammalian hibernation and arousal. J. Comp. Physiol. B. 180:775-783<br />
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|year=2010<br />
|journal=J. Comp. Physiol. B<br />
|abstract=Hibernation elicits a major reduction in whole-animal O(2) consumption that corresponds with active suppression of liver mitochondrial electron transport capacity at, or downstream of, succinate dehydrogenase (SDH). During arousal from the torpor phase of hibernation this suppression is reversed and metabolic rates rise dramatically. In this study, we used the 13-lined ground squirrel (Ictidomys tridecemlineatus) to assess isolated liver mitochondrial respiration during the torpor phase of hibernation and various stages of arousal to elucidate a potential role of SDH in metabolic suppression. State 3 and state 4 respiration rates were seven- and threefold lower in torpor compared with the summer-active and interbout euthermic states. Respiration rates increased during arousal so that when body temperature reached 30 degrees C in late arousal, state 3 and state 4 respiration were 3.3- and 1.8-fold greater than during torpor, respectively. SDH activity was 72% higher in interbout euthermia than in torpor. Pre-incubating with isocitrate [to alleviate oxaloacetate (OAA) inhibition] increased state 3 respiration rate during torpor by 91%, but this rate was still fourfold lower than that measured in interbout euthermia. Isocitrate pre-incubation also eliminated differences in SDH activity among hibernation bout stages. OAA concentration correlated negatively with both respiration rates and SDH activity. These data suggest that OAA reversibly inhibits SDH in torpor, but cannot fully account for the drastic metabolic suppression observed during this hibernation phase.<br />
|keywords=Hibernation , Arousal, Mitochondria, Succinate dehydrogenase, Oxaloacetate<br />
}}<br />
{{Labeling<br />
|discipline=Mitochondrial Physiology<br />
|organism=Other Mammal<br />
|tissues=Hepatocyte; Liver<br />
|preparations=Isolated Mitochondria<br />
|enzymes=Complex II; Succinate Dehydrogenase<br />
}}</div>Oroboroshttps://wiki.oroboros.at/index.php?title=Armstrong_2010_J_Comp_Physiol_B&diff=12212Armstrong 2010 J Comp Physiol B2011-03-14T12:54:16Z<p>Oroboros: </p>
<hr />
<div>{{Publication<br />
|title=Armstrong C. and Staples J.F. 2010. The role of succinate dehydrogenase and oxaloacetate in mitochondrial metabolism during mammalian hibernation and arousal. J. Comp. Physiol. B. 180:775-783<br />
|info=[http://www.ncbi.nlm.nih.gov/pubmed/20112024 PMID:20112024]<br />
|authors=Armstrong C, Staples J<br />
|year=2010<br />
|journal=J. Comp. Physiol. B<br />
|abstract=Hibernation elicits a major reduction in whole-animal O(2) consumption that corresponds with active suppression of liver mitochondrial electron transport capacity at, or downstream of, succinate dehydrogenase (SDH). During arousal from the torpor phase of hibernation this suppression is reversed and metabolic rates rise dramatically. In this study, we used the 13-lined ground squirrel (Ictidomys tridecemlineatus) to assess isolated liver mitochondrial respiration during the torpor phase of hibernation and various stages of arousal to elucidate a potential role of SDH in metabolic suppression. State 3 and state 4 respiration rates were seven- and threefold lower in torpor compared with the summer-active and interbout euthermic states. Respiration rates increased during arousal so that when body temperature reached 30 degrees C in late arousal, state 3 and state 4 respiration were 3.3- and 1.8-fold greater than during torpor, respectively. SDH activity was 72% higher in interbout euthermia than in torpor. Pre-incubating with isocitrate [to alleviate oxaloacetate (OAA) inhibition] increased state 3 respiration rate during torpor by 91%, but this rate was still fourfold lower than that measured in interbout euthermia. Isocitrate pre-incubation also eliminated differences in SDH activity among hibernation bout stages. OAA concentration correlated negatively with both respiration rates and SDH activity. These data suggest that OAA reversibly inhibits SDH in torpor, but cannot fully account for the drastic metabolic suppression observed during this hibernation phase.<br />
|keywords=Hibernation , Arousal, Mitochondria, Succinate dehydrogenase, Oxaloacetate<br />
}}<br />
{{Labeling<br />
|discipline=Mitochondrial Physiology<br />
|organism=Other Mammal<br />
|tissues=Hepatocyte; Liver<br />
|preparations=Isolated Mitochondria<br />
|enzymes=Complex II; Succinate Dehydrogenase<br />
}}<br />
__showfactbox__</div>Oroboroshttps://wiki.oroboros.at/index.php?title=Allen_MiP2010&diff=12202Allen MiP20102011-03-14T12:02:32Z<p>Oroboros: </p>
<hr />
<div>{{Abstract<br />
|title=Allen AM, Graham A (2010) Acute mitochondrial dysfunction inhibits macrophage cholesterol efflux to apolipoprotein AI.<br />
|info=[http://www.mitophysiology.org/index.php?mip2010-session1 Abstracts Session 1]<br />
|authors=Allen AM, Graham A<br />
|year=2010<br />
|event=MiP2010<br />
|abstract=Mitochondrial cholesterol trafficking, from the outer mitochondrial membrane to sterol 27-hydroxylase located on the inner mitochondrial membrane, facilitates generation of endogenous oxysterol ligands, capable of activating Liver X receptor (LXR) responsive genes such as ATP binding cassette transporters (ABCA1, ABCG1, ABCG4) which orchestrate cholesterol efflux from cells (1,2).<br />
|articletype=MiPNet-online Publication, MiPsociety-Publication<br />
}}<br />
{{Labeling|articletype=MiPNet-online Publication, MiPsociety-Publication<br />
}}<br />
==Full text==<br />
<br />
Mitochondrial cholesterol trafficking, from the outer mitochondrial membrane to sterol 27-hydroxylase located on the inner mitochondrial membrane, facilitates generation of endogenous oxysterol ligands, capable of activating Liver X receptor (LXR) responsive genes such as ATP binding cassette transporters (ABCA1, ABCG1, ABCG4) which orchestrate cholesterol efflux from cells (1,2). The first step in this pathway is critically regulated by ABCA1, in combination with lipid-poor acceptor apolipoproteins such as apoAI or apoE, while ABCG1 and ABCG4 transfer cholesterol to nascent HDL, so that these transporters act in concert to generate cholesterol-rich HDL. In this study, we explore the hypothesis that mitochondrial dysfunction, hallmark of developing atherosclerotic lesions, contributes to the accumulation of excess cholesterol within arterial macrophage ‘foam’ cells, by negatively impacting on the athero-protective cholesterol efflux pathway.<br />
<br />
Macrophage (RAW264.7) mitochondrial function was pharmacologically modified, in acute incubations (3 h) to avoid overt toxicity, using antimycin A, which inhibits Complex III (CIII), dinitrophenol, which dissipates mitochondrial membrane potential ΔΨmt, nigericin, which alters mitochondrial ΔpH, and oligomycin, which inhibits CV. Cell viability was assessed by lactate dehydogenase (LDH) release, mitochondrial function assessed by dimethylthiazolyl diphenyltetrazolium bromide (MTT) conversion to formazan, total cellular ATP levels measured using CellTitre-Glo Bioluminescent assay and ΔΨmt measured via tetramethyl rhodamine ethyl ester (TMRE) binding. Quantitative PCR used to measure expression of key enzymes and transporters linked with cholesterol homeostasis, and measurement of (3H)cholesterol efflux to apoAI (20 µg∙ml-1) or HDL (20 µg∙ml-1) were performed as previously described (3).<br />
<br />
Stimulation of murine RAW 264.7 macrophages with dibutyryl cyclic AMP (0.3mM) induced (3H) cholesterol efflux to apoAI by up to 5-fold (P<0.001) and to HDL by up to 3.5-fold (P<0.05), as previously (3). Acute incubation with oligomycin (3 h) significantly reduced (53%; P<0.01) cholesterol efflux to apoAI (right), whereas efflux to HDL remained consistently unaffected by this inhibitor. Oligomycin also induced a reduction in ΔΨmt (39%; P<0.05), while total cellular levels of ATP and release of cytosolic LDH remained unchanged during this period. Cholesterol efflux to both apoAI and HDL appeared inhibited by nigericin, although this proved significant only for apoAI (39%; P<0.01); however, this compound also reduced cellular levels of ATP (28%; P<0.01) and ΔΨmt (18%, P<0.5) during the incubation period. By contrast, cholesterol efflux to either apoAI or HDL remained unchanged following addition of dinitrophenol (10 µM) or antimycin A (10 µM) to the culture medium; these compounds did not alter ΔΨmt, total cellular ATP levels or LDH release during this short incubation period, although loss of mitochondrial function was evident after 24 h, or at higher concentrations of drug. Notably, acute treatment with oligomycin (10 µM) altered the expression of genes implicated in cholesterol homeostasis: expression of Hmgcr (3.9 fold; P<0.05) and Srebpf2 (3.4-fold; P<0.05) increased under basal conditions, while paradoxically both Abca1 and Ldlr expression increased by 16.6-fold (P<0.05) and 3.4-fold (P<0.05) respectively, following cholesterol efflux to apoAI; together, these data suggest integration of mitochondrial function with macrophage cholesterol homeostasis mechanisms.<br />
<br />
In summary, changes in ΔΨmt, or intra-mitochondrial ATP levels, may be key factors regulating macrophage cholesterol homeostasis and efflux via ABCA1 to apoAI. The mechanisms involved remain unexplored, at present, but may provide targets for novel therapeutic strategies.<br />
<br />
1. Venkateswaran A, Laffitte BA, Joseph SB, Mak PA, Wilpitz DC, Edwards PA, Tontonoz P. (2000) Control of cellular cholesterol efflux by the nuclear oxysterol receptor LXRalpha. Proc. Natl Acad. Sci USA 97: 12097-12102.<br />
<br />
2. Oram JF, Vaughan AM (2006) ATP-binding cassette cholesterol transporters and cardiovascular disease. Circ. Res. 99: 1031-1043.<br />
<br />
3. Taylor JM, Borthwick F, Bartholomew C, Graham A (2010) Over-expression of steroidogenic acute regulatory protein (StAR) increases macrophage cholesterol efflux to apolipoprotein AI. Cardiovasc. Res. cvq015.</div>Oroboroshttps://wiki.oroboros.at/index.php?title=Template:Abstract&diff=12199Template:Abstract2011-03-14T11:49:07Z<p>Oroboros: </p>
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[[Category:Abstracts]]</div>Oroboroshttps://wiki.oroboros.at/index.php?title=Template:MitoPedia_topics&diff=12196Template:MitoPedia topics2011-03-14T11:13:00Z<p>Oroboros: </p>
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<hr />
<div>{{MitoPedia<br />
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</includeonly></div>Oroboroshttps://wiki.oroboros.at/index.php?title=Form:Bioblast&diff=12188Form:Bioblast2011-03-14T11:02:18Z<p>Oroboros: Reverted edits by Oroboros (talk) to last revision by Wiethuechter Anita</p>
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| Permeabilization agent = [[List of permeabilization agents |Permeabilization agent]]<br />
}}[[MitoPedia topic::x| ]]}}&nbsp;}}<br />
</includeonly></div>Oroboroshttps://wiki.oroboros.at/index.php?title=ET_capacity&diff=12185ET capacity2011-03-14T10:45:44Z<p>Oroboros: </p>
<hr />
<div>{{MitoPedia<br />
|abbr=''E''<br />
|description=Respiratory [[ETS|electron transfer system]] capacity, ''E'', of mitochondria in the experimentally induced [[non-coupled]] (fully uncoupled) state, in [[mitochondrial preparations]] with defined substrates, or in intact cells, by titration of an established [[uncoupler]] to optimum concentration at maximum flux. Non-coupled respiration yields an estimate of '''ETS capacity'''. In this state ''E'', the [[mt-membrane potential]] is collapsed, which provides a reference state for [[flux control ratio]]s and measurement of mt-membrane potential.<br />
|info=[[MiPNet12.15]], [[Gnaiger_2009_IJBCB]], [[List of respiratory states]]<br />
|type=Respiration<br />
}}<br />
{{MitoPedia topics<br />
|mitopedia topic=Respiratory state<br />
|type=Respiration<br />
}}<br />
==Why not State 3u?==<br />
[[Talk:ETS capacity]]</div>Oroboroshttps://wiki.oroboros.at/index.php?title=ET_capacity&diff=12184ET capacity2011-03-14T10:45:22Z<p>Oroboros: </p>
<hr />
<div>{{MitoPedia<br />
|abbr=''E''<br />
|description=Respiratory [[ETS|electron transfer system]] capacity, ''E'', of mitochondria in the experimentally induced [[non-coupled]] (fully uncoupled) state, in [[mitochondrial preparations]] with defined substrates, or in intact cells, by titration of an established [[uncoupler]] to optimum concentration at maximum flux. Non-coupled respiration yields an estimate of '''ETS capacity'''. In this state ''E'', the [[mt-membrane potential]] is collapsed, which provides a reference state for [[flux control ratio]]s and measurement of mt-membrane potential.<br />
|info=[[MiPNet12.15]], [[Gnaiger_2009_IJBCB]], [[List of respiratory states]]<br />
|type=Respiration<br />
}}<br />
{{MitoPedia topics|type=Respiration<br />
}}<br />
==Why not State 3u?==<br />
[[Talk:ETS capacity]]</div>Oroboros