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2.

Figure 3. Proapoptotic and antiapoptotic Bcl regulated mitochondrial signaling mediates PM-induced oxidative stress and apoptosis in CF. From: AIR POLLUTION INDUCES ENHANCED MITOCHONDRIAL OXIDATIVE STRESS IN CYSTIC FIBROSIS AIRWAY EPITHELIUM.

PM upregulated proapoptotic proteins BAD, Bax, p53 and p21; and enhanced mitochondrial localization of Bax; while, antiapoptotic Bcl-2, Bcl-xl, Mcl-1 and Xiap were unchanged (). Over expression of antiapoptotic Bcl-xl inhibited PM-induced apoptosis (). *p<0.05 control vs. PM; † p<0.05 WT vs. Bcl-xl; n=3.

O Kamdar, et al. FEBS Lett. ;582(25-26):3601-3606.
3.

Figure 2. ROS mediated mitochondrial signaling in CF epithelium. From: AIR POLLUTION INDUCES ENHANCED MITOCHONDRIAL OXIDATIVE STRESS IN CYSTIC FIBROSIS AIRWAY EPITHELIUM.

PM enhanced ROS generation in IB3-1 cells as compared to S9 cells; while, mitochondrial inhibitors, DIDS, Rotenone and TTFA blocked PM-induced ROS and apoptosis as assessed by TUNEL and DNA Fragmentation ELISA (). *p<0.05 control vs. PM; † and ‡ p<0.05 PM vs. Inhibitor + PM; ¶p<0.05 S9 cells vs. IB3-1 cells PM; §p<0.05 S9 cells control vs. IB3-1 cells control; n=3.

O Kamdar, et al. FEBS Lett. ;582(25-26):3601-3606.
4.

Figure 1. PM enhanced apoptosis in human CF bronchial epithelium via mitochondrial pathway. From: AIR POLLUTION INDUCES ENHANCED MITOCHONDRIAL OXIDATIVE STRESS IN CYSTIC FIBROSIS AIRWAY EPITHELIUM.

PM (25µg/cm2) caused 6-fold increase in DNA fragmentation in IB3-1 cells as compare to 3.5-fold in the S9 and normal HBE cells (). PM induced significant reduction in mitochondrial membrane potential and caused caspase-9, caspase-3 and PARP-1 activation in IB3-1 cells as compare to S9 cells, suggesting enhanced mitochondrial signaling in CF (). Mean ± SEM, *p<0.05 control vs. PM, †p<0.05 S9 cells vs. IB3-1 cells PM, ‡p<0.05 S9 cells control vs. IB3-1 cells control, n=3.

O Kamdar, et al. FEBS Lett. ;582(25-26):3601-3606.

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