Basic & Clinical Medicine ›› 2014, Vol. 34 ›› Issue (3): 295-300.
Previous Articles Next Articles
Received:
Revised:
Online:
Published:
Abstract: Objective To observe the effects of erythropoietin ( EPO) on angiotensinⅡ ( AngⅡ ) induced neonatal rat cardiomyocyte hypertrophy and its signal protein expression. Methods Cardiomyocytes were isolated from new-born Sprague-Dawley rats and were used to establish the model of hypertrophy by AngII in vitro.The cells was treated with EPO or/and P38MAPK inhibitor SB203580. The cell surface area, [3H]-leucine incorporation ,mRNA expression of atrial natriuretic factor(ANF) and β-myosin heavy chain(β-MHC) of cardiomyocytes were employed to detect cardiomyocyte hypertrophy. The mRNA levels of TGF-β1 and P38MAPK was analyzed by real-time quantitative PCR. The protein expression of TGF-β1、TAK1、P38MAPK and phosphorylation of TAK1 and P38MAPK were analyzed by Western blot. Results EPO attenuated hypertrophy of cardiomyocytes. EPO significantly suppressed TGF-β1、TAK1、P38MAPK、phosphrylation of TAK1 and P38MAPK expression. SB203580 represses cardiac hypertrophy. Conclusions EPO attenuates cardiomyocytes hypertrophy induced by Ang II,and it might be associated with TGF β1-TAK1-P38MAPK signaling pathway.
Key words: erythropoietin,cardiocyte hypertrophy,TGF-β1,TAK1,p38MAPK
CLC Number:
R542.2
0 / / Recommend
Add to citation manager EndNote|Reference Manager|ProCite|BibTeX|RefWorks
URL: http://journal11.magtechjournal.com/Jwk_jcyxylc/EN/
http://journal11.magtechjournal.com/Jwk_jcyxylc/EN/Y2014/V34/I3/295