Testosterone induces cardiomyocyte hypertrophy in rats and upregulates the expression of ERK1/2 / 基础医学与临床

ABSTRACT

Objective To explore the role of ERK1/2 protein in development of myocardial hypertrophy.Methods Myocardial cells were isolated from ventricles of 1～3-day-old neonate rats and purifed by a culture method.Neonate rat cardiomyocyte hypertrophic responses were assayed by measuring protein content,protein synthesis rate and cell surface area.Expression of protein ERK1/2 were detected by Western blot.Results Cell protein content,~3H-leucine(~3 H-Leu)incorporation and cell surface area increased by treating of cardiomyocytes with T(10~(-10)～10~(-6) mol/L)for 24 h.The maxium effect was observed at the concentration of 10~(-8) mol/L.The increase of cell protein content induced by T was inhibited by pretreating with flutamide(10~(-5) mol/L)for 2 h,while there was no effect on cardiomyocytes pretreating with flutamide alone.The increase of ~3H-Leu incorporation induced by T was blocked by PD98059(50 μmol/L).Expression of ERK1/2 was upregulated significantly by treating with testoster one for 24 h at the level of 10~(-8) mol/L.The increased expression of ERK1/2 induced by T was reversed by pretreating with flutamide(10~(-5) mol/L)for 2 h.Conclusion T with physio-concentration may induce cardiomyocyte hypertrophy and this effect was possibly mediated through the activation of ERK1/2 signalling.During this procession,T upregulated the protein expression of ERK1/2 mediated by androgen receptor.