Difference between revisions of "Chen 2020 Chem Biol Interact"
(Created page with "{{Publication |title=Chen HY, Ho YJ, Chou HC, Liao EC, Tsai YT, Wei YS, Lin LH, Lin MW, Wang YS, Ko ML, Chan H (2020) TGF-β1 signaling protects retinal ganglion cells from ox...") |
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|title=Chen HY, Ho YJ, Chou HC, Liao EC, Tsai YT, Wei YS, Lin LH, Lin MW, Wang YS, Ko ML, Chan H (2020) TGF-β1 signaling protects retinal ganglion cells from oxidative stress via modulation of the HO-1/Nrf2 pathway. Chem Biol Interact [Epub ahead of print]. | |title=Chen HY, Ho YJ, Chou HC, Liao EC, Tsai YT, Wei YS, Lin LH, Lin MW, Wang YS, Ko ML, Chan H (2020) TGF-β1 signaling protects retinal ganglion cells from oxidative stress via modulation of the HO-1/Nrf2 pathway. Chem Biol Interact [Epub ahead of print]. | ||
|info=[https://www.ncbi.nlm.nih.gov/pubmed/32980322 PMID: 32980322] | |info=[https://www.ncbi.nlm.nih.gov/pubmed/32980322 PMID: 32980322] | ||
|authors=Chen | |authors=Chen Hsin-Yi, Ho Yi-Jung, Chou Hsiu-Chuan, Liao En-Chi, Tsai Yi-Ting, Wei Yu-Shan, Lin Li-Hsun, Lin Meng-Wei, Wang Yi-Shiuan, Ko Mei-Lan, Chan Hong-Lin | ||
|year=2020 | |year=2020 | ||
|journal=Chem Biol Interact | |journal=Chem Biol Interact | ||
|abstract=Oxidative stress provides a major contribution to the pathogenesis of glaucoma and may induce retinal ganglion cell (RGC) damage. Transforming growth factor β (TGF-β) has appeared as a neuroprotective protein in various indignities. However, the TGF-β mechanism of protective effects against oxidative stress damage in RGCs still undetermined. In our research, we investigated the regulatory mechanisms and potential effects of TGF-β1 & TGF-β2 in hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>)-stimulated oxidative stress of RGCs in vitro. By a series of cell functional qualitative analysis, such as MTT cell viability assay, wound healing ability assay, apoptosis assay, intracellular ROS detection, immunoblot analysis, intracellular GSH content, and high-resolution respirometry, we illustrated the cell state in oxidative stress-induced injury. Results of protein expression showed that TGF-β1 & TGF-β2 was upregulated in RGCs after H<sub>2</sub>O<sub>2</sub> stimulation. Cell functional assays resulted that knockdown of TGF-β1 & TGF-β2 reduced survival rate whereas enhanced apoptosis and accumulation of reactive oxygen species (ROS). Especially TGF-β1 upregulation promoted the protein expression of aldehyde dehydrogenase 3A1 (ALDH3A1) and increased the activity of antioxidant and neuroprotection pathways. Additionally, TGF-β1 & TGF-β2 on antioxidant signaling was related to activation of heme oxygenase-1 (HO-1) and nuclear factor erythroid 2-related factor (Nrf2), which are stress-response proteins. ROS accumulation followed by the accumulation of hypoxia-inducible factor (HIF-1α) caused mitochondrial damage and led to neurodegeneration. In summary, our results demonstrated that TGF-β1 preserves RGCs from free radicals-mediated injury by upregulating the activation of Nrf2 expression and HO-1 signaling balance HIF-1α upregulation, implying a prospective role of TGF-β1 in retinal neuroprotection-related therapies. | |abstract=Oxidative stress provides a major contribution to the pathogenesis of glaucoma and may induce retinal ganglion cell (RGC) damage. Transforming growth factor β (TGF-β) has appeared as a neuroprotective protein in various indignities. However, the TGF-β mechanism of protective effects against oxidative stress damage in RGCs still undetermined. In our research, we investigated the regulatory mechanisms and potential effects of TGF-β1 & TGF-β2 in hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>)-stimulated oxidative stress of RGCs ''in vitro''. By a series of cell functional qualitative analysis, such as MTT cell viability assay, wound healing ability assay, apoptosis assay, intracellular ROS detection, immunoblot analysis, intracellular GSH content, and high-resolution respirometry, we illustrated the cell state in oxidative stress-induced injury. Results of protein expression showed that TGF-β1 & TGF-β2 was upregulated in RGCs after H<sub>2</sub>O<sub>2</sub> stimulation. Cell functional assays resulted that knockdown of TGF-β1 & TGF-β2 reduced survival rate whereas enhanced apoptosis and accumulation of reactive oxygen species (ROS). Especially TGF-β1 upregulation promoted the protein expression of aldehyde dehydrogenase 3A1 (ALDH3A1) and increased the activity of antioxidant and neuroprotection pathways. Additionally, TGF-β1 & TGF-β2 on antioxidant signaling was related to activation of heme oxygenase-1 (HO-1) and nuclear factor erythroid 2-related factor (Nrf2), which are stress-response proteins. ROS accumulation followed by the accumulation of hypoxia-inducible factor (HIF-1α) caused mitochondrial damage and led to neurodegeneration. In summary, our results demonstrated that TGF-β1 preserves RGCs from free radicals-mediated injury by upregulating the activation of Nrf2 expression and HO-1 signaling balance HIF-1α upregulation, implying a prospective role of TGF-β1 in retinal neuroprotection-related therapies. | ||
|keywords=HO-1/Nrf2 pathway, Oxidative stress, Retinal ganglion cells, TGF-β1 | |keywords=HO-1/Nrf2 pathway, Oxidative stress, Retinal ganglion cells, TGF-β1 | ||
|editor=[[Plangger M]] | |editor=[[Plangger M]] | ||
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{{Labeling | {{Labeling | ||
|area=Respiration | |area=Respiration | ||
|injuries=Oxidative stress;RONS | |||
|organism=Mouse | |||
|tissues=Nervous system | |||
|preparations=Intact cells | |||
|couplingstates=LEAK, ROUTINE, ET | |||
|pathways=ROX | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|additional=2020-10 | |additional=2020-10 | ||
}} | }} |
Revision as of 21:43, 1 October 2020
Chen HY, Ho YJ, Chou HC, Liao EC, Tsai YT, Wei YS, Lin LH, Lin MW, Wang YS, Ko ML, Chan H (2020) TGF-β1 signaling protects retinal ganglion cells from oxidative stress via modulation of the HO-1/Nrf2 pathway. Chem Biol Interact [Epub ahead of print]. |
Chen Hsin-Yi, Ho Yi-Jung, Chou Hsiu-Chuan, Liao En-Chi, Tsai Yi-Ting, Wei Yu-Shan, Lin Li-Hsun, Lin Meng-Wei, Wang Yi-Shiuan, Ko Mei-Lan, Chan Hong-Lin (2020) Chem Biol Interact
Abstract: Oxidative stress provides a major contribution to the pathogenesis of glaucoma and may induce retinal ganglion cell (RGC) damage. Transforming growth factor β (TGF-β) has appeared as a neuroprotective protein in various indignities. However, the TGF-β mechanism of protective effects against oxidative stress damage in RGCs still undetermined. In our research, we investigated the regulatory mechanisms and potential effects of TGF-β1 & TGF-β2 in hydrogen peroxide (H2O2)-stimulated oxidative stress of RGCs in vitro. By a series of cell functional qualitative analysis, such as MTT cell viability assay, wound healing ability assay, apoptosis assay, intracellular ROS detection, immunoblot analysis, intracellular GSH content, and high-resolution respirometry, we illustrated the cell state in oxidative stress-induced injury. Results of protein expression showed that TGF-β1 & TGF-β2 was upregulated in RGCs after H2O2 stimulation. Cell functional assays resulted that knockdown of TGF-β1 & TGF-β2 reduced survival rate whereas enhanced apoptosis and accumulation of reactive oxygen species (ROS). Especially TGF-β1 upregulation promoted the protein expression of aldehyde dehydrogenase 3A1 (ALDH3A1) and increased the activity of antioxidant and neuroprotection pathways. Additionally, TGF-β1 & TGF-β2 on antioxidant signaling was related to activation of heme oxygenase-1 (HO-1) and nuclear factor erythroid 2-related factor (Nrf2), which are stress-response proteins. ROS accumulation followed by the accumulation of hypoxia-inducible factor (HIF-1α) caused mitochondrial damage and led to neurodegeneration. In summary, our results demonstrated that TGF-β1 preserves RGCs from free radicals-mediated injury by upregulating the activation of Nrf2 expression and HO-1 signaling balance HIF-1α upregulation, implying a prospective role of TGF-β1 in retinal neuroprotection-related therapies. • Keywords: HO-1/Nrf2 pathway, Oxidative stress, Retinal ganglion cells, TGF-β1 • Bioblast editor: Plangger M
Labels: MiParea: Respiration
Stress:Oxidative stress;RONS Organism: Mouse Tissue;cell: Nervous system Preparation: Intact cells
Coupling state: LEAK, ROUTINE, ET
Pathway: ROX
HRR: Oxygraph-2k
2020-10