Difference between revisions of "Bir 2013 Abstract MiP2013"
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{{Abstract | {{Abstract | ||
|title=Bir A, Sen O, Anand S, Banerjee P, Sahoo A, Khemka V, Cappai R, Chakrabarti S (2013) Ī±-Synuclein mediated alterations in mitochondrial oxidative phosphorylation system: Implications in the pathogenesis of Parkinsonās disease. Mitochondr Physiol Network 18.08. | |title=Bir A, Sen O, Anand S, Banerjee P, Sahoo A, Khemka V, Cappai R, Chakrabarti S (2013) Ī±-Synuclein mediated alterations in mitochondrial oxidative phosphorylation system: Implications in the pathogenesis of Parkinsonās disease. Mitochondr Physiol Network 18.08. | ||
|info=[http://www.mitophysiology.org/?MiP2013 MiP2013] | |||
|authors=Bir A, Sen O, Anand S, Banerjee P, Sahoo A, Khemka V, Cappai R, Chakrabarti S | |authors=Bir A, Sen O, Anand S, Banerjee P, Sahoo A, Khemka V, Cappai R, Chakrabarti S | ||
|year=2013 | |year=2013 | ||
|event=MiP2013 | |event=MiP2013 Programme | ||
|abstract=[[File:BirA.jpg|right|200px|Aritri Bir]] | |abstract=[[File:BirA.jpg|right|200px|Aritri Bir]] | ||
Ī±-Synucleinopathy and mitochondrial dysfunction are important elements of sporadic Parkinsonās disease (PD) pathogenesis [1]. It is, however, not clear whether the accumulated Ī±-synuclein in degenerating dopaminergic neurons in PD causes mitochondrial injury and subsequent cell death. Our earlier study has shown that Ī±-synuclein causes functional impairment of rat brain mitochondria incubated in vitro [2]. | Ī±-Synucleinopathy and mitochondrial dysfunction are important elements of sporadic Parkinsonās disease (PD) pathogenesis [1]. It is, however, not clear whether the accumulated Ī±-synuclein in degenerating dopaminergic neurons in PD causes mitochondrial injury and subsequent cell death. Our earlier study has shown that Ī±-synuclein causes functional impairment of rat brain mitochondria incubated in vitro [2]. |
Revision as of 19:38, 10 September 2013
Bir A, Sen O, Anand S, Banerjee P, Sahoo A, Khemka V, Cappai R, Chakrabarti S (2013) Ī±-Synuclein mediated alterations in mitochondrial oxidative phosphorylation system: Implications in the pathogenesis of Parkinsonās disease. Mitochondr Physiol Network 18.08. |
Link: MiP2013
Bir A, Sen O, Anand S, Banerjee P, Sahoo A, Khemka V, Cappai R, Chakrabarti S (2013)
Event: MiP2013 Programme
Ī±-Synucleinopathy and mitochondrial dysfunction are important elements of sporadic Parkinsonās disease (PD) pathogenesis [1]. It is, however, not clear whether the accumulated Ī±-synuclein in degenerating dopaminergic neurons in PD causes mitochondrial injury and subsequent cell death. Our earlier study has shown that Ī±-synuclein causes functional impairment of rat brain mitochondria incubated in vitro [2].
Mitochondrial membrane potential was measured using the carbocyanine dye JC1, and the phosphorylation capacity determined spectrophotometrically from inorganic phosphate utilization [2,3]. The respiratory functions of mitochondria in isolated preparations and within intact cells were analyzed by high-resolution respirometry. Ī±-Synuclein accumulation within SHSY5Y cells was induced by lactacystin treatment and detected by immunoblotting. The transfection of SHSY5Y cells with Ī± synuclein specific SiRNA was carried out using the lipofectamine kit (Invitrogen).
Our results show that Ī±-synuclein causes a loss of membrane potential and phosphorylation capacity with alterations in respiratory parameters in isolated rat brain mitochondria. Some of these effects were inhibited very significantly by cyclosporine (1 Ī¼M). When SHSY5Y cells were exposed to 5 Ī¼M lactacystin for 24 h, Ī±-synuclein accumulation occured intracellularly as detected by immunoblotting experiments. Further, lactacystin treatment of SHSY5Y cells also leads to mitochondrial dysfunction and cell death concomitant with Ī± synuclein accumulation. To confirm the involvement of Ī± synuclein in lactacystin induced mitochondrial dysfunction, the effects of cyclosporine and the gene silencing of Ī±-synuclein with specific SiRNA on these phenomena are being investigated.
ā¢ O2k-Network Lab: IN Kolkata Chakrabarti S
Labels: MiParea: Respiration, mt-Medicine Pathology: Neurodegenerative, Parkinson's Stress:Cell death Organism: Rat Tissue;cell: Nervous system Preparation: Intact cells, Isolated Mitochondria"Isolated Mitochondria" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property.
Regulation: mt-Membrane potential Coupling state: OXPHOS
HRR: Oxygraph-2k
SHSY5Y cells, MiP2013, S09
Affiliations and author contributions
1 - Dept of Biochemistry, Institute of Postgraduate Medical Education and Research, Kolkata, India;
2 - Dept of Pathology and Bio21 Molecular Science and Biotechnology Institute, University of Melbourne, Victoria, Australia.
Email: [email protected]
References
- Beal MF (2004) Commentary on āāAlpha-synuclein and mitochondria: a tangled skeinā. Exp Neurol 186: 109ā111.
- Banerjee K, Sinha M, Pham Cle L, Jana S, Chanda D, Cappai R, Chakrabarti S (2010) Alpha-synuclein induced membrane depolarization and loss of phosphorylation capacity of isolated rat brain mitochondria: Implications in Parkinsonās disease. FEBS Lett 584: 1571-1576.
- Bagh MB, Thakurta IG, Biswas M, Behera P, Chakrabarti S (2011) Age-related oxidative decline of mitochondrial functions in rat brain is prevented by long term oral antioxidant supplementation. Biogerontology 12: 119-131.