DC Field | Value | Language |
---|---|---|
dc.contributor.advisor | Chung, An-Sik | - |
dc.contributor.advisor | 정안식 | - |
dc.contributor.author | Kim, Bu-Yeo | - |
dc.contributor.author | 김부여 | - |
dc.date.accessioned | 2011-12-12T07:53:02Z | - |
dc.date.available | 2011-12-12T07:53:02Z | - |
dc.date.issued | 2001 | - |
dc.identifier.uri | http://library.kaist.ac.kr/search/detail/view.do?bibCtrlNo=165708&flag=dissertation | - |
dc.identifier.uri | http://hdl.handle.net/10203/27497 | - |
dc.description | 학위논문(박사) - 한국과학기술원 : 생물과학과, 2001.2, [ viii, 85 p. ] | - |
dc.description.abstract | Reactive oxygen species (ROS) have emerged as important signaling molecules in the regulation of various cellular processes. In our study, we investigated the effect of a wide range of ROS on Chinese hamster lung fibroblast (V79) cell proliferation. Treatment with $H_2O_2$, superoxide anion (generated by xanthine and xanthine oxidase), menadione and phenazine methosulfate increased the cell proliferation by approximately 50%. Moreover, a similar result was observed after partial inhibition of superoxide dismutase (SOD) and glutathione peroxidase. This up-regulation of cell proliferation was suppressed by pre-treatment with hydroxyl radical scavengers and iron chelating agents. In addition to ROS, treatment with exogenous catalase and SOD mimic (MnTMPyP) suppressed the normal cell proliferation. Short-term exposure of the cells to 100 micro M $H_2O_2$ was sufficient to induce proliferation, which indicated that activation of the signaling pathway is important as an early event. Accordingly, we assessed the ability of $H_2O_2$ to activate mitogen-activated protein kinases (MAPK). Jun-N-terminal kinase (JNK) and p38 MAPK were both rapidly and transiently activated by 100 μM H2O2, with maximal activation 30 minutes after treatment. The binding activity of AP-1 and the phosphorylation of c-Jun were also increased at the same time. However, the activity of extracellular signal-regulated kinase (ERK) was not changed. Pretreatment with SB203580 and SB202190, specific inhibitors of p38 MAPK, reduced the cell proliferation induced by $H_2O_2$. The activation of both JNK and p38 MAPK were also suppressed by pre-treatment with hydroxyl radical scavenger and iron chelating agent. These results suggest that the trace metal-driven Fenton reaction is a critical mechanism that underlies cell proliferation and MAPK activation. Further, the receptor tyrosine kinase, protein kinase C, and phospholipase $A_2$ pathways might be at least partially involved in the activation of JNK, p... | eng |
dc.language | eng | - |
dc.publisher | 한국과학기술원 | - |
dc.subject | proliferation | - |
dc.subject | reactive oxygen species | - |
dc.subject | fibroblast | - |
dc.subject | 섬유아 세포 | - |
dc.subject | 세포성장 | - |
dc.subject | 활성산소 | - |
dc.title | Effects of reactive oxygen species on proliferation of Chinese hamster lung fibroblast (V79) cells | - |
dc.title.alternative | 활성산소가 Chinese hamster 폐 섬유아 세포의 성장에 미치는 영향 | - |
dc.type | Thesis(Ph.D) | - |
dc.identifier.CNRN | 165708/325007 | - |
dc.description.department | 한국과학기술원 : 생물과학과, | - |
dc.identifier.uid | 000965061 | - |
dc.contributor.localauthor | Chung, An-Sik | - |
dc.contributor.localauthor | 정안식 | - |
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