Effect of urotensin Ⅱ on hypertrophy of cardiac myocytes from neonatal SD rats
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Effect of urotensin Ⅱ on hypertrophy of cardiac myocytes from neonatal SD rats
Journal of Army Medical UniversityVol. 30, Issue 24, Pages: 2293-2295(2008)
作者机构:
第三军医大学新桥医院心血管内科,全军心血管病研究所
作者简介:
基金信息:
DOI:
CLC:R322.11;R329.24;R977.1
Published:2008,
Published Online:30 December 2008,
稿件说明:
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LI WEI, LI AI-MIN, GUO RUI-WEI, et al. Effect of urotensin Ⅱ on hypertrophy of cardiac myocytes from neonatal SD rats. [J]. Journal of army medical university, 2008, 30(24): 2293-2295.
DOI:
LI WEI, LI AI-MIN, GUO RUI-WEI, et al. Effect of urotensin Ⅱ on hypertrophy of cardiac myocytes from neonatal SD rats. [J]. Journal of army medical university, 2008, 30(24): 2293-2295.DOI:
Effect of urotensin Ⅱ on hypertrophy of cardiac myocytes from neonatal SD rats
mol/L U Ⅱ处理心肌细胞12、24、48 h,随着时间增加,心肌细胞β-MHC、CaN mRNA和蛋白表达呈递增趋势,其中处理24 h组与正常对照组有显著差异 (
P
<
0.05);③预先用环胞素A 5μmol/L(cyclosporin A CsA)处理正常心肌细胞24 h,然后用10
-8
mol/L U Ⅱ作用24 h,心肌细胞β-MHC、CaN mRNA和蛋白表达与正常心肌细胞经10
-8
mol/L U Ⅱ单纯作用24 h差异有显著意义(
P
<
0.05)。 结论 U Ⅱ能够诱导心肌细胞的肥大
环胞素A(CsA)能阻断此效应,CaN参与了U Ⅱ诱导的心肌肥大过程。
Abstract
Objective To explore the mechanism by which urotensin Ⅱ induces hypertrophy of the cultured rat cardiomyocytes. Methods The cultured cardiomyocytes from neonatal SD rats were treated with urotensin Ⅱ
also with cyclosporine A for its blocking effect on urotensin Ⅱ induced cardiomyocytes hypertrophy. The mRNA and protein levels of β-MHC and CaN were evaluated by real-tim
e PCR and Western blotting
respectively. Results In the cells treated with 10
-8
and 10
-7
mol/L urotensin Ⅱ
the mRNA and protein levels of β-MHC and CaN were significantly higher than that of control (
P
<
0.05). Treatment of cardiomyocytes with 10
-8
mol/L urotensin Ⅱ for 12-48 h induced a time-dependent increase of β-MHC and CaN mRNA and protein expressions (
P
<
0.05). Urotensin Ⅱ-induced upregulation of β-MHC and CaN mRNA and protein expressions can be abated by 24-hour cyclosporine A pretreatment (
P
<
0.05). Conclusion Urotensin Ⅱ can induce cardiomyocytes hypertrophy and cyclosporine A can block this effect. CaN participates in this process. Our results may contribute to the investigation of cardiaomyocyts hypertrophy induced by hypertension and other cardiac diseases.
Cardiomyocyte hypertrophy induced by indoxyl sulfate in vitro
G protein-coupled bile acid receptor 1 activation attenuates endothelin-1-induced rat cardiomyocyte hypertrophy by inhibiting CaN/NAFT3 pathway
Cyclosporin A promotes axon growth of cortical neurons by inhibiting calcineurin activity
Role of protein kinase C in adenosine A1 receptor regulating opening of mitochondria permeability transition pore in hypoxic cardiac myocytes
Cardiac myocyte damage in fetus of rabbits with intrahepatic cholestasis pregnant
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