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.

We studied the effects of fibroblast growth factor (FGF‐10) on H2O2‐induced alveolar epithelial cell (AEC) G1 arrest and the role of G1 cyclins. FGF‐10 prevented H2O2‐induced AEC G1 arrest. FGF‐10 induced 2–4‐fold increase in cyclin E, cyclin A and CDKs (2, 4) alone and in AEC treated with H2O2. H2O2 downregulated cyclin D1; FGF‐10 blocked these effects. FGF‐10 prevented H2O2‐induced upregulation of CDK inhibitor, p21. SiRNAp21 blocked H2O2‐induced downregulation of cyclins, CDKs and AEC G1 arrest. Accordingly, we provide first evidence that FGF‐10 regulates G1 cyclins and CDKs, and prevents H2O2‐induced AEC G1 arrest.