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15-Deoxy-Δ12,14-prostaglandin J2 rescues PC12 cells from H2O2-induced apoptosis through Nrf2-mediated upregulation of heme oxygenase-1: Potential roles of Akt and ERK1/2

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dc.contributor.authorKim, Ji-Woo-
dc.contributor.authorLi, Mei-Hua-
dc.contributor.authorJang, Jung-Hee-
dc.contributor.authorNa, Hye-Kyung-
dc.contributor.authorSong, Na-Young-
dc.contributor.authorLee, Chan-
dc.contributor.authorJohnson, Jeffrey A.-
dc.contributor.authorSurh, Young-Joon-
dc.date.accessioned2021-01-31T09:21:58Z-
dc.date.available2021-01-31T09:21:58Z-
dc.date.issued2008-12-
dc.identifier.citationBiochemical Pharmacology, Vol.76 No.11, pp.1577-1589-
dc.identifier.issn0006-2952-
dc.identifier.other3042-
dc.identifier.urihttps://hdl.handle.net/10371/172608-
dc.description.abstractOxidative stress induced by reactive oxygen intermediates has been implicated in a variety of human diseases including rheumatoid arthritis and neuro degenerative disorders. 15-Deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)), a terminal dehydration product of prostaglandin D(2), is an endogenous ligand of peroxisome proliferator-activated receptor-gamma and exhibits a number of biological activities including the proapoptotic activity. Recent studies have revealed that this cyclopentenone prostaglandin, at non-toxic concentrations, can also exert antiapoptotic or cytoprotective effects. In this study, the underlying mechanisms involved in the protective effects of 15d-PGJ(2) on the H(2)O(2)-induced cytotoxicty were explored using cultured rat pheochromocytoma (PC12) cells. PC12 cells treated with H(2)O(2) underwent apoptosis, which was attenuated by pretreatment with non-toxic concentrations of 15d-PGJ(2). Treatment of the PC12 cells with 15d-PGJ(2) resulted in increased nuclear translocation, DNA-binding and transcriptional activity of NF-E2-related factor 2 (Nrf2), leading to upregulation of heme oxygenase-1 (HO-1) expression, which provided an adaptive survival response against the H(2)O(2)-derived oxidative cytotoxicity. Transfection of PC12 cells with dominant-negative Nrf2 gene abolished the 15d-PGJ(2)-derived induction of HO-1 expression. Moreover, the 15d-PGJ(2)-mediated increases in Nrf2-ARE binding and ARE luciferase activity were suppressed by the dominant-negative mutation as well as the pharmacological inhibition of Akt/protein kinase B or extracellular signal-regulated kinase 1/2 (ERK1/2). Taken together, these findings suggest that 15d-PGJ(2) augments cellular antioxidant defense capacity through activation of Akt and ERK signal pathways that leads to Nrf2 activation, and subsequently HO-1 induction, thereby protecting the PC12 cells from H(2)O(2)-induced oxidative cell death. (c) 2008 Published by Elsevier Inc.-
dc.subject15-Deoxy-Delta(12,14)-prostaglandin J(2)-
dc.subjectHeme oxygenase-1-
dc.subjectNrf2-
dc.subjectAntioxidant response elements-
dc.subjectCyclopentenone prostaglandin-
dc.title15-Deoxy-Δ12,14-prostaglandin J2 rescues PC12 cells from H2O2-induced apoptosis through Nrf2-mediated upregulation of heme oxygenase-1: Potential roles of Akt and ERK1/2-
dc.typeArticle-
dc.contributor.AlternativeAuthor서영준-
dc.identifier.doi10.1016/j.bcp.2008.08.007-
dc.citation.journaltitleBiochemical Pharmacology-
dc.identifier.scopusid2-s2.0-55949091956-
dc.citation.endpage1589-
dc.citation.number11-
dc.citation.startpage1577-
dc.citation.volume76-
dc.identifier.urlhttps://www.sciencedirect.com/science/article/pii/S0006295208005534?via%3Dihub-
dc.identifier.rimsid3042-
dc.identifier.sci000261569400028-
dc.contributor.affiliatedAuthorSurh, Young-Joon-
Appears in Collections:
Graduate School of Convergence Science and Technology (융합과학기술대학원)Dept. of Molecular and Biopharmaceutical Sciences (분자의학 및 바이오제약학과)Journal Papers (저널논문_분자의학 및 바이오제약학과)
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