Objective To study estrogen receptor (ER) ? and ? expression in the newborn and adult rats,and effect of estrogen on ER? and ER? in ovariectomized rat heart.Methods By RT-PCR and Western blot analysis,changes in ER? and ER? in newborn and adult rat heart chambers were investigated,and subsequently,the effect of 17?-estradiol deficit and supplementation on ER? and ER?,and heart chamber wieght and ratio to body weight in ovariectomized rats were evaluated.Results ER? mRNA was lower in all heart chambers of newborn rats,but was elevated by 3-to 20-fold in the atria and ventricles of adult rats,these differences were efficiently translated into 67?kD ER? protein.Inversely,ER? mRNA expressed in the heart chambers of newborn rats was higher,and was dramatically decreased by 2-to 7-fold in all heart chambers of adult rats.In adult rats,ovariectomy decreased atrial ER? mRNA and ER? protein expression,and the atrial weight and atria/body weight ratio. Treatment with 17?-estradiol in ovariectomized rats reversed these changes;meanwhile these changes showed the dose-dependent relation to some extent along with the increment of 17?-estradiol dosage,but ovariectomy and treatment with 17?-estradiol did not alter the atria ER? mRNA expression,and the heart,ventricle ratio to body weight.Conclusion ERs expression is different between the newborn and adult rat heart,ER? may play an important role than ER? in the development of the rat heart,ER? high expression suggests that it functions as a predominant estrogenic mediator in adult heart.Estrogen mainly targets the atria;and activates atrio-myocyte proliferation via ER? mediated mechanism.

Objective To study the effect of 17?-estradial(E-2) on apoptosis of cardiomyocytes induced by norepinephrine(NE) in vitro and its mechanism. Methods The cultured neonatal rat cardiomyocytes were treated with NE(50??mol/L),E-2(10?nmol/L) or NE(50??mol/L)+E-2(10?nmol/L) respectively in serum-free DMEM for 48?h.The morphological changes of myocytes were studied by phase-microscopy and transmission electron microscopy;apoptosis was identified by DNA laddering and apoptotic rate was assayed by flow cytometer;cfos protein in cardiomyocytes was detected using semiquantitative immunofluorescence cytochemistry technique. Results 17?-estradiol inhibited the morphological changes of apoptotic cardiomyocytes induced by norepinephine such as cell atrophy,condensed chromatin clumps against the nuclear envelope associated with swelling of mitochondria and presentation of apoptotic body,DNA laddering disappeared,the apoptotic rate decreased and the expression of c-fos protein inhibited in cardiomyocytes.Conclusion 17?-estradiol can protect cultured cardiomyocytes from apoptosis induced by norepinephrine,its mechanism might associate with suppression of c-fos protein expression.

Objective To observe effects of 17?-estradiol on phenylephrine-induced hypertrophy in cultured neonatal rat cardiomyocytes and to explore its mechanisms. Methods Using cultured neonatal rat cardiomyocytes treated with different factors as a model,surface area of cardiomyocytes was measured by computer photograph analysis software;the protein synthesis rate was assayed with leucine intake method;the proto-oncogene c-fos protein expression was assessed with immunocytochemistry technique;the markers of cardiomyocyte hypertrophy,embryonic genes such as ?-MHC\,?-skA and ANP mRNA expressions were assessed with semiquantitative reverse transcription-PCR. Results 17?-estradiol inhibited obviously phenylephrine-induced increase of surface area and the protein synthesis rate of cardiomyocytes,reduced c-fos protein expression of hypertrophic cardiomyocytes,and down-regulated ?-MHC、?-skA mRNA expressions and up-regulated ANP mRNA expression.Conclusion 17?-estradiol inhibits hypertrophy of cardiomyocytes and its mechanisms might be related with the suppression of c-fos protein expression,the reversion of the embryonic switching of contractile protein genes(?MHC and ?-skA),the increase of ANP mRNA expression.