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Bim mediates mitochondria‐regulated particulate matter‐induced apoptosis in alveolar epithelial cells
Author(s) -
Zhang J.,
Ghio A.J.,
Chang W.,
Kamdar O.,
Rosen G.D.,
Upadhyay D.
Publication year - 2007
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2007.07.080
Subject(s) - apoptosis , microbiology and biotechnology , mitochondrion , downregulation and upregulation , chemistry , bcl 2 family , caspase , programmed cell death , biology , biochemistry , gene
We studied the role of Bim, a pro‐apoptotic BCL‐2 family member in Airborne particulate matter (PM 2.5 μm)‐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.

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