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Carbon monoxide produced by heme oxygenase-1 in response to nitrosative stress induces expression of glutamate-cysteine ligase in PC12 cells via activation of phosphatidylinositol 3-kinase and Nrf2 signaling
DC Field | Value | Language |
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dc.contributor.author | Li, Mei-Hua | - |
dc.contributor.author | Jang, Jung-Hee | - |
dc.contributor.author | Na, Hye-Kyung | - |
dc.contributor.author | Cha, Young-Nam | - |
dc.contributor.author | Surh, Young-Joon | - |
dc.date.accessioned | 2021-01-31T10:15:51Z | - |
dc.date.available | 2021-01-31T10:15:51Z | - |
dc.date.created | 2017-11-15 | - |
dc.date.issued | 2007-09 | - |
dc.identifier.citation | Journal of Biological Chemistry, Vol.282 No.39, pp.28577-28586 | - |
dc.identifier.issn | 0021-9258 | - |
dc.identifier.other | 3368 | - |
dc.identifier.uri | https://hdl.handle.net/10371/172768 | - |
dc.description.abstract | Induction of heme oxygenase-1 (HO-1) expression has been associated with adaptive cytoprotection against a wide array of toxic insults, but the underlying molecular mechanisms remain largely unresolved. In this study, we investigated the potential role of carbon monoxide(CO), one of the by-products of the HO-1reaction, in the adaptive survival response to peroxynitrite-induced PC12 cell death. Upon treatment of rat pheochromocytoma (PC12) cells with the peroxynitrite generator 3-morpholinosydnonimine hydrochloride (SIN-1), the cellular GSH level decreased initially, but was gradually restored to the basal level. This was accompanied by increased expression of the catalytic subunit of glutamate-cysteine ligase (GCLC), the rate-limiting enzyme in GSH biosynthesis. The SIN-1-induced GCLC up-regulation was preceded by induction of HO-1 and subsequent CO production. Inhibition of HO activity by zinc protoporphyrin IX or knockdown of HO-1 gene expression by small interfering RNA abrogated the up-regulation of GCLC expression and the subsequent GSH restoration induced by SIN-1. In contrast, additional exposure to the CO-releasing molecule (CO-RM) restored the GSH level previously reduced by inhibition of CO production using zinc protoporphyrin IX. Furthermore, CO-RM treatment up-regulated GCLC expression through activation of Nrf2. The CO-RM-induced activation of Nrf2 was under the control of the phosphatidylinositol 3-kinase/Akt signaling pathway. In conclusion, CO produced by HO-1 rescues PC12 cells from nitrosative stress through induction of GCLC, which is mediated by activation of phosphatidylinositol 3-kinase/Akt and subsequently Nrf2 signaling. | - |
dc.language | 영어 | - |
dc.publisher | American Society for Biochemistry and Molecular Biology Inc. | - |
dc.title | Carbon monoxide produced by heme oxygenase-1 in response to nitrosative stress induces expression of glutamate-cysteine ligase in PC12 cells via activation of phosphatidylinositol 3-kinase and Nrf2 signaling | - |
dc.type | Article | - |
dc.contributor.AlternativeAuthor | 서영준 | - |
dc.identifier.doi | 10.1074/jbc.M701916200 | - |
dc.citation.journaltitle | Journal of Biological Chemistry | - |
dc.identifier.wosid | 000249642100032 | - |
dc.identifier.scopusid | 2-s2.0-35348981179 | - |
dc.citation.endpage | 28586 | - |
dc.citation.number | 39 | - |
dc.citation.startpage | 28577 | - |
dc.citation.volume | 282 | - |
dc.identifier.sci | 000249642100032 | - |
dc.description.isOpenAccess | Y | - |
dc.contributor.affiliatedAuthor | Surh, Young-Joon | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.subject.keywordPlus | GAMMA-GLUTAMYLCYSTEINE SYNTHETASE | - |
dc.subject.keywordPlus | HUMAN NEUROBLASTOMA-CELLS | - |
dc.subject.keywordPlus | SMOOTH-MUSCLE-CELLS | - |
dc.subject.keywordPlus | PROTEIN-KINASE-C | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | NITRIC-OXIDE | - |
dc.subject.keywordPlus | GENE-EXPRESSION | - |
dc.subject.keywordPlus | INTRACELLULAR GLUTATHIONE | - |
dc.subject.keywordPlus | NF-E2-RELATED FACTOR-2 | - |
dc.subject.keywordPlus | TRANSCRIPTION FACTOR | - |
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