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Carbon monoxide protects PC12 cells from peroxynitrite-induced apoptotic death by preventing the depolarization of mitochondrial transmembrane potential
DC Field | Value | Language |
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dc.contributor.author | Li, Mei-Hua | - |
dc.contributor.author | Cha, Young-Nam | - |
dc.contributor.author | Surh, Young-Joon | - |
dc.date.accessioned | 2021-01-31T10:14:23Z | - |
dc.date.available | 2021-01-31T10:14:23Z | - |
dc.date.created | 2017-11-15 | - |
dc.date.issued | 2006-04 | - |
dc.identifier.citation | Biochemical and Biophysical Research Communications, Vol.342 No.3, pp.984-990 | - |
dc.identifier.issn | 0006-291X | - |
dc.identifier.other | 3752 | - |
dc.identifier.uri | https://hdl.handle.net/10371/172750 | - |
dc.description.abstract | Heme oxygenase-1 (HO-1), the rate-limiting enzyme in catalyzing heme degradation into biliverdin, free iron, and carbon monoxide (CO), serves as a protective enzyme against oxidative and nitrosative stresses. In the present study, we investigated the cytoprotective effects of HO-1 upregulation and its product CO against the peroxynitrite-induced PC12 cell death. PC12 cells treated with 3-morphoinosydonimine (SIN-1), a generator of peroxynitrite (ONOO-), underwent apoptotic cell death as evidenced by dissipation of mitochondrial transmembrane potential (Delta psi m), release of mitochondrial cytochrome e into cytoplasm, cleavage of poly(ADP-ribose)polymerase and fragmentation of internucleosomal DNA. Pretreatment of PC12 cells with a low non-toxic concentration of SIN-1 (0.5 mM) induced HO-1 expression and abrogated the cell death caused by subsequent challenge with high dose SIN-1 (2.5 mM). Furthermore, pretreatment of PC12 cells with SnCl,, a potent inducer of HO-1 expression, increased endogenous production of CO (HO activity) and rescued the PC12 cells from peroxynitrite-induced apoptosis. The cytoprotective effect of SnCl2 was abolished when the HO activity was inhibited by zinc protoporphyrin IX (ZnPP IX). PC12 cells treated directly with the CO-releasing molecule, tricarbonyldichlororuthenium (II) dimer ([Ru(CO)(3)Cl-2](2)) became tolerant to the depolarization of Delta psi m and apoptosis induced by high dose peroxynitrite. Taken together, these data demonstrate that the adaptive protection against peroxynitrite-induced apoptotic death in PC12 cells is mediated by CO formed as a consequence of HO-I induction. (c) 2006 Elsevier Inc. All rights reserved. | - |
dc.language | 영어 | - |
dc.publisher | Academic Press | - |
dc.title | Carbon monoxide protects PC12 cells from peroxynitrite-induced apoptotic death by preventing the depolarization of mitochondrial transmembrane potential | - |
dc.type | Article | - |
dc.contributor.AlternativeAuthor | 서영준 | - |
dc.identifier.doi | 10.1016/j.bbrc.2006.02.046 | - |
dc.citation.journaltitle | Biochemical and Biophysical Research Communications | - |
dc.identifier.wosid | 000236168600042 | - |
dc.identifier.scopusid | 2-s2.0-33644618423 | - |
dc.citation.endpage | 990 | - |
dc.citation.number | 3 | - |
dc.citation.startpage | 984 | - |
dc.citation.volume | 342 | - |
dc.identifier.sci | 000236168600042 | - |
dc.description.isOpenAccess | N | - |
dc.contributor.affiliatedAuthor | Surh, Young-Joon | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.subject.keywordPlus | SENSITIVE POTASSIUM CHANNELS | - |
dc.subject.keywordPlus | SMOOTH-MUSCLE-CELLS | - |
dc.subject.keywordPlus | HEME OXYGENASE-1 | - |
dc.subject.keywordPlus | NITRIC-OXIDE | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | INDUCED CYTOTOXICITY | - |
dc.subject.keywordPlus | UP-REGULATION | - |
dc.subject.keywordPlus | INDUCTION | - |
dc.subject.keywordPlus | RAT | - |
dc.subject.keywordPlus | INVOLVEMENT | - |
dc.subject.keywordAuthor | heme oxygenase-1 | - |
dc.subject.keywordAuthor | carbon monoxide | - |
dc.subject.keywordAuthor | carbon monoxide-releasing molecule | - |
dc.subject.keywordAuthor | peroxynitrite | - |
dc.subject.keywordAuthor | anti-apoptosis | - |
dc.subject.keywordAuthor | PC12 cells | - |
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