Involvement of p38 mitogen-activated protein kinase and apoptosis signal-regulating kinase-1 in nitric oxide-induced cell death in PC12 cells
- Authors
- Han, Ok-Jin; Joe, Keun Ho; Kim, Seong Won; Lee, Hee Sung; Kwon, Nyoun Soo; Baek, Kwang Jin; Yun, Hye-Young
- Issue Date
- May-2001
- Publisher
- KLUWER ACADEMIC/PLENUM PUBL
- Keywords
- nitric oxide; p38 MAPK; ASK1; cell death; PC12
- Citation
- NEUROCHEMICAL RESEARCH, v.26, no.5, pp 525 - 532
- Pages
- 8
- Journal Title
- NEUROCHEMICAL RESEARCH
- Volume
- 26
- Number
- 5
- Start Page
- 525
- End Page
- 532
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/25221
- DOI
- 10.1023/A:1010917129951
- ISSN
- 0364-3190
1573-6903
- Abstract
- Although nitric oxide (NO) plays key signaling roles in the nervous systems, excess NO leads to cell death. In this study, the involvement of p38 mitogen-activated protein kinase (p38 MAPK) and apoptosis signal-regulating kinase-1 (ASK1) in NO-induced cell death was investigated in PC12 cells. NO donor transiently activated p38 MAPK in the wild type parental PC12 cells, whereas the p38 MAPK activation was abolished in NO-resistant PC12 cells (PC12-NO-R). p38 MAPK inhibitors protected the cells against NO-induced death, whereas the inhibitors were not significantly protective against the cytotoxicity of reactive oxygen species. Stable transfection with dominant negative p38 MAPK mutant reduced NO-induced cell death. Stable transfection with dominant negative mutant of ASK1 attenuated NO-stimulated activation of p38 MAPK and decreased NO-induced cell death. These results suggest that p38 MAPK and its upstream regulator ASK1 are involved in NO-induced PC12 cell death.
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