期刊
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY
卷 55, 期 1, 页码 96-105出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/FJC.0b013e3181c9548b
关键词
CaMKII; angiotensin II; electrical field stimulation; extracellular matrix; cardiac fibrosis; fibroblast
资金
- Natural Science Foundation of Jiangsu Province [BK2007064]
Calcium-calmodulin-dependent protein kinase II (CaMKI) is one of the main protein kinases mediating intracellular Ca2+ changes. It is also involved in the process of cardiac diseases, Such as cardiac hypertrophy, but its effects on myocardial fibrosis remain unclear. The present study investigates whether CaMKII is involved in cardiac fibroblast proliferation and extracellular matrix (ECM) secretion induced by angiotensin II (AngII) or electrical field stimulation (EFS) in Cultured neonatal rat cardiac fibroblasts. Cardiac fibroblast proliferation was assessed by a cell Survival assay (MTT) and manual cell enumeration. Cellular matrix production was demonstrated by matrix metalloproteinases (MMP) 1, 2, 9, and collagen I/III messenger RNA expression, MMP-2, 9 protein expression, and secretion of transforming growth factor beta(1) and tumor necrosis factor alpha. Either AngII or EFS promoted cardiac fibroblast proliferation and ECM secretion, while also up-regulating expression of CaMKII delta B and delta C. More importantly, CaMKII inhibitors, autocamtide-2-related inhibitory peptide (A I P 5 mu M) or KN93 (0.5 mu M), suppressed cardiac fibroblast proliferation, inhibited the excretion of transforming growth factor beta(1) and tumor necrosis factor alpha, decreased the messenger RNA expression of MMP-1, 2, 9 and collagen I/III, and decreased the protein expression of MMP-2, 9. These results suggest that CaMKII mediates cardiac fibroblast proliferation and ECM secretion induced by either AngII or EFS.
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