期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 344, 期 3, 页码 900-905出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2006.04.013
关键词
neutral sphingomyelinase 2; apoptosis; hydrogen peroxide; glutathione; ceramide; lung
资金
- NHLBI NIH HHS [T32 HL-07013, HL-71871, HL-66189, R01 HL066189, R01 HL071871, T32 HL007013] Funding Source: Medline
We have previously shown that accumulation of ceramide, triggered by hydrogen peroxide (H2O2), induces apoptosis of human airway epithelial (HAE) cells. Under oxidant exposure, a lung sphingomyelinase (SMase) is activated and displays continued ceramide generation and pro-apoptotic signaling, thus leading to the pathological apoptosis that causes lung injury. In a search for a specific SMase that is modulated by oxidative stress, we recently cloned nSMase2 from monkey lung tissue and HAE cells. Here, we show that this nSMase2 is up-regulated by an oxidant (H2O2) and is inhibited by an antioxidant (glutathione (GSH)). Moreover, nSMase2 subcellular localization is governed by oxidant exposure, which leads to its preferential trafficking to the plasma membrane, where it generates ceramide and induces apoptosis. On the other hand, exposure to GSH results in nSMase2 trafficking to the nucleus, where it neither generates ceramide nor induces apoptosis. (c) 2006 Elsevier Inc. All rights reserved.
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