期刊
GENE
卷 583, 期 1, 页码 8-14出版社
ELSEVIER
DOI: 10.1016/j.gene.2016.02.039
关键词
UII; Cardiomyocyte hypertrophy; CaMKII; PLN; SERCA 2a
资金
- Natural Science Foundation of Shanxi Province [2012011036-1]
- Shanxi Provincial Scientific Research Projects Foundation of Abroad-Studying Personnel [2012-7]
- Shanxi Provincial University Scientific Research Projects Foundation of Abroad-Studying and Returning Personnel [2011-63]
- Selected Scientific Research Projects Foundation of Abroad-Studying Personnel, Office of Human Resources, Shanxi Province [2013-68]
- Selected Scientific Research Projects Foundation of Abroad-Studying and Returning Personnel, Shanxi Province [2010-97]
- Technology Innovation Foundation of Shanxi Medical University [2010-7, 01200912]
- Shanxi Provincial Scientific Research Projects Foundation of Abroad-Studying and Returning Personnel [2009-9]
- Shanxi Provincial University Scientific Research Projects Foundation of Abroad-Studying Personnel [201128]
- Shanxi Provincial Technology Projects Foundation of Abroad-Studying Personnel [2012-084]
Although studies have shown that Urotensin II (UII) can induce cardiomyocyte hypertrophy and UII-induced cardiomyocyte hypertrophy model has been widely used for hypertrophy research, but its precise mechanism remains unknown. Recent researches have demonstrated that UII-induced cardiomyocyte hypertrophy has a relationship with the changes of intracellular Ca2+ concentration. Therefore, the aim of this study was to investigate the mechanisms of cardiomyocyte hypertrophy induced by UII and to explore whether the calcium/calmodulin-dependent protein kinase II (CaMKII)-mediated up-regulating of phospholamban (PLN) Thr17-phosphorylation signaling pathway contributed to UII-induced cardiomyocyte hypertrophy. Primary cultures of neonatal rat cardiomyocytes were stimulated for 48 h with UII. Cell size, protein/DNA contents and intracellular Ca2+ were determined. Phosphorylated and total forms of CaMKII, PLN and the total amount of serco/endo-plasmic reticulum ATPases (SERCA 2a) were quantified by western blot. The responses of cardiomyocytes to UII were also evaluated after pretreatment with the CaMKII inhibitor, KN-93. These results showed that UII increased cell size, protein/DNA ratio and intracellular Ca2+, consistent with a hypertrophic response. Furthermore, the phosphorylation of CaMKII and its downstream target PLN (Thr17), SERCA 2a levels were up-regulated by UII treatment. Conversely, treatment with KN-93 reversed all those effects of UII. Taken together, the results suggest that UII can induce cardiomyocyte hypertrophy through CaMKII-mediated up-regulating of PLN Thr17-phosphorylation signaling pathway. (C) 2016 Elsevier B.V. All rights reserved.
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