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Bim mediates mitochondria-regulated particulate matter-induced apoptosis in alveolar epithelial cells

We studied the role of Bim, a pro-apoptotic BCL-2 family member in Airborne particulate matter (PM 2.5μm)-induced apoptosis in alveolar epithelial cells (AEC). PM induced AEC apoptosis by causing significant reduction of mitochondrial membrane potential and increase in caspase-9, caspase-3 and PARP-...

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Bibliographic Details
Published in:FEBS letters 2007-09, Vol.581 (22), p.4148-4152
Main Authors: Zhang, J., Ghio, A.J., Chang, W., Kamdar, O., Rosen, G.D., Upadhyay, D.
Format: Article
Language:English
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Summary:We studied the role of Bim, a pro-apoptotic BCL-2 family member in Airborne particulate matter (PM 2.5μm)-induced apoptosis in alveolar epithelial cells (AEC). PM induced AEC apoptosis by causing significant reduction of mitochondrial membrane potential and increase in caspase-9, caspase-3 and PARP-1 activation. PM upregulated pro-apoptotic protein Bim and enhanced translocation of Bim to the mitochondria. ShRNABim blocked PM-induced apoptosis by preventing activation of the mitochondrial death pathway suggesting a role of Bim in the regulation of mitochondrial pathway in AEC. Accordingly, we provide the evidence that Bim mediates PM-induced apoptosis via mitochondrial pathway.
ISSN:0014-5793
1873-3468
DOI:10.1016/j.febslet.2007.07.080