Abstract
We studied the role of Bim, a pro-apoptotic BCL-2 family member in Airborne particulate matter (PM 2.5 microm)-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.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Apoptosis / drug effects*
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Apoptosis Regulatory Proteins / genetics
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Apoptosis Regulatory Proteins / metabolism*
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Bcl-2-Like Protein 11
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Cattle
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Cell Line, Tumor
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DNA Fragmentation / drug effects
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Epithelial Cells / cytology*
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Epithelial Cells / drug effects*
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Humans
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Membrane Proteins / genetics
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Membrane Proteins / metabolism*
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Mitochondria / metabolism*
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Models, Biological
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Particulate Matter / pharmacology*
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Poly(ADP-ribose) Polymerases / genetics
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Proto-Oncogene Proteins / genetics
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Proto-Oncogene Proteins / metabolism*
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Pulmonary Alveoli / cytology*
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Pulmonary Alveoli / drug effects
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RNA, Small Interfering / metabolism
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Rats
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Up-Regulation / drug effects
Substances
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Apoptosis Regulatory Proteins
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BCL2L11 protein, human
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Bcl-2-Like Protein 11
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Bcl2l11 protein, rat
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Membrane Proteins
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Particulate Matter
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Proto-Oncogene Proteins
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RNA, Small Interfering
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Poly(ADP-ribose) Polymerases