@article{APS8149,
author = {Wen-Lan Liu and Xun Guo and Zhao-Gui Guo},
title = {Effects of p38 and p42/p44 CCDPK signaling on H2O2-induced apoptosis in bovine aortic endothelial cells},
journal = {Acta Pharmacologica Sinica},
volume = {21},
number = {11},
year = {2016},
keywords = {},
abstract = {\"AIM:
To investigate the effects of p38 and p42/p44 Ca(2+)-calmodulin dependent protein kinases (CCDPK) signaling on hydroperoxide (H2O2)-induced apoptosis in cultured bovine aortic endothelial cells (BAEC).
METHODS:
Morphologic changes and quantification of apoptotic cells were determined under fluorescence microscope after a 24-h treatment of BAEC by H2O2. Cell viability was determined with MTT method. DNA fragmentation was visualized by agarose gel electrophoresis. The expression of phospho-p38 and phospho-p42/p44 CCDPK was measured by Western blotting.
RESULTS:
H2O2 elicited typical apoptotic morphologic changes (chromatic condensation, nucleus fragmentation) and DNA fragmentation. At 100-500 mumol.L-1, incubation of BAEC with H2O2 for 24 h also induced phospho-p38 and phospho-p42/p44 CCDPK expression in a concentration-dependent manner. Interestingly, H2O2-induced apoptosis was markedly increased by preincubation with U0126, a specific p42/p44 CCDPK inhibitor. However, SB203580, a specific p38 CCDPK inhibitor, enhanced the expression of phospho-p42/p44 CCDPK induced by H2O2, but had no effect on BAEC survival.
CONCLUSION:
p42/p44 CCDPK signaling appears to play protective roles in H2O2-induced apoptosis in BAEC, whereas p38 CCDPK is not the main signaling pathway mediating H2O2-induced cellular apoptosis.\"},
issn = {1745-7254}, url = {http://www.chinaphar.com/article/view/8149}
}