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dc.contributor.author Kang, Hojin ko
dc.contributor.author Khang, Rin ko
dc.contributor.author Ham, Sangwoo ko
dc.contributor.author Jeong, Ga Ram ko
dc.contributor.author Kim, Hyojung ko
dc.contributor.author Jo, Minkyung ko
dc.contributor.author Lee, Byoung Dae ko
dc.contributor.author Lee, Yun Il ko
dc.contributor.author Jo, Areum ko
dc.contributor.author Park, ChiHu ko
dc.contributor.author Kim, Hyein ko
dc.contributor.author Seo, Jeongkon ko
dc.contributor.author Paek, Sun Ha ko
dc.contributor.author Lee, Yun-Song ko
dc.contributor.author Choi, Jeong-Yun ko
dc.contributor.author Lee, Yunjong ko
dc.contributor.author Shin, Joo-Ho ko
dc.date.available 2017-09-11T03:33:04Z -
dc.date.created 2017-09-01 -
dc.date.issued 2017-07 -
dc.identifier.citation Oncotarget, v.8, no.30, pp.48603 - 48618 -
dc.identifier.issn 1949-2553 -
dc.identifier.uri http://hdl.handle.net/20.500.11750/4404 -
dc.description.abstract Progressive dopaminergic neurodegeneration is responsible for the canonical motor deficits in Parkinson's disease (PD). The widely prescribed anti-diabetic medicine metformin is effective in preventing neurodegeneration in animal models; however, despite the significant potential of metformin for treating PD, the therapeutic effects and molecular mechanisms underlying dopaminergic neuroprotection by metformin are largely unknown. In this study, we found that metformin induced substantial proteomic changes, especially in metabolic and mitochondrial pathways in the substantia nigra (SN). Consistent with this data, metformin increased mitochondrial marker proteins in SH-SY5Y neuroblastoma cells. Mitochondrial protein expression by metformin was found to be brain region specific, with metformin increasing mitochondrial proteins in the SN and the striatum, but not the cortex. As a potential upstream regulator of mitochondria gene transcription by metformin, PGC-1α promoter activity was stimulated by metformin via CREB and ATF2 pathways. PGC-1α and phosphorylation of ATF2 and CREB by metformin were selectively increased in the SN and the striatum, but not the cortex. Finally, we showed that metformin protected dopaminergic neurons and improved dopamine-sensitive motor performance in an MPTP-induced PD animal model. Together these results suggest that the metformin-ATF2/CREBPGC- 1α pathway might be promising therapeutic target for PD. © Kang et al. -
dc.language English -
dc.publisher Impact Journals LLC -
dc.subject 2 Parts -
dc.subject Alpha Synuclein -
dc.subject Brain -
dc.subject Dopaminergic -
dc.subject Dopaminergic -
dc.subject Gerotarget -
dc.subject Knockout Mice -
dc.subject Metformin -
dc.subject Metformin -
dc.subject Mitochondria -
dc.subject Mitochondria -
dc.subject Mouse Model -
dc.subject MPTP -
dc.subject Parkinson&apos -
dc.subject s Disease -
dc.subject Parkinson&apos -
dc.subject s Disease -
dc.subject PGC 1 Alpha -
dc.subject PGC 1 Alpha -
dc.subject PGC 1 Alpha -
dc.subject Phosphorylation -
dc.subject Protein Kinase -
dc.title Activation of the ATF2/CREB-PGC-1 alpha pathway by metformin leads to dopaminergic neuroprotection -
dc.type Article -
dc.identifier.doi 10.18632/oncotarget.18122 -
dc.identifier.wosid 000406232400010 -
dc.identifier.scopusid 2-s2.0-85025826408 -
dc.type.local Article(Overseas) -
dc.type.rims ART -
dc.description.journalClass 1 -
dc.contributor.nonIdAuthor Kang, Hojin -
dc.contributor.nonIdAuthor Khang, Rin -
dc.contributor.nonIdAuthor Ham, Sangwoo -
dc.contributor.nonIdAuthor Jeong, Ga Ram -
dc.contributor.nonIdAuthor Kim, Hyojung -
dc.contributor.nonIdAuthor Jo, Minkyung -
dc.contributor.nonIdAuthor Lee, Byoung Dae -
dc.contributor.nonIdAuthor Jo, Areum -
dc.contributor.nonIdAuthor Park, ChiHu -
dc.contributor.nonIdAuthor Kim, Hyein -
dc.contributor.nonIdAuthor Seo, Jeongkon -
dc.contributor.nonIdAuthor Paek, Sun Ha -
dc.contributor.nonIdAuthor Lee, Yun-Song -
dc.contributor.nonIdAuthor Choi, Jeong-Yun -
dc.contributor.nonIdAuthor Lee, Yunjong -
dc.contributor.nonIdAuthor Shin, Joo-Ho -
dc.identifier.citationVolume 8 -
dc.identifier.citationNumber 30 -
dc.identifier.citationStartPage 48603 -
dc.identifier.citationEndPage 48618 -
dc.identifier.citationTitle Oncotarget -
dc.type.journalArticle Article -
dc.description.isOpenAccess N -
dc.contributor.affiliatedAuthor Lee, Yun Il -
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