Objective To investigate the effects of basic helix-loop-helix family member e41(BHLHE41)on angiotensin Ⅱ(Ang Ⅱ)-induced hypertrophy and apoptosis of H9C2 cardiomyocytes.Methods The expression level of BHLHE41 stimulated by Ang Ⅱ was investigated,and the cells were divided into normal group and Ang Ⅱ group.To investigate the effect of silencing BHLHE41(siBHLHE41)on cardiomyocyte hypertrophy and apoptosis,the cells were divided into 4groups:blank group[transfected with small in-terfering RNA(siRNA)+phosphate buffered saline(PBS)],siBHLHE41 group[transfected with siBHLHE41+PBS],model group(transfected with siRNA+Ang Ⅱ)and experimental group(transfected with siBHLHE41+Ang Ⅱ).The mRNA levels of BHLHE41,β-myosin heavy chain(β-MHC),atrial natriuretic peptide(ANP),B-type natriuretic peptide(BNP),poly ADP-ribose polymer-ase(PARP),B-cell lymphoma-2(Bcl-2),B-cell lymphoma-2-associated X protein(Bax),and p53 were detected by real-time fluorescence quantitative polymerase chain reaction(RT-qPCR).The protein expression levels of BHLHE41,Bax,Bcl-2,PARP and p53 were detected by Western blot.Phalloidin staining was used to observe the surface area of cardiomyocytes,TUNEL staining was used to observe cardiomyocytes apoptosis.Results Compared with the normal group,the mRNA and protein expression levels of BHL-HE41 was higher in the Ang Ⅱ group.Compared with blank group,the mRNA expression levels of β-MHC,ANP,BNP in the model group were upregulated,and the protein and mRNA expression levels of PARP,Bax and p53 in model group were significantly increased,the expression level of Bcl-2 was significantly decreased,the surface area of cardiomyocytes was significantly increased,and the apopto-sis rate of cardiomyocytes was significantly increased(P＜0.05).Compared with model group,the mRNA expression levels of β-MHC,ANP and BNP in the experimental group were upregulated,and the protein and mRNA expression levels of PARP,Bax and p53 in experi-mental group were significantly increased,the expression level of Bcl-2 was significantly decreased,the surface area of cardiomyocytes was increased,and the apoptosis rate of cardiomyocytes was significantly increased(P＜0.05).Conclusion Silencing BHLHE41 can aggravate Ang Ⅱ-induced hypertrophy and apoptosis of H9C2 cardiomyocytes,which may be related to the p53 activation of the apoptotic signaling pathway.

Objective To investigate the effects of basic helix-loop-helix family member e41(BHLHE41)on angiotensin Ⅱ(Ang Ⅱ)-induced hypertrophy and apoptosis of H9C2 cardiomyocytes.Methods The expression level of BHLHE41 stimulated by Ang Ⅱ was investigated,and the cells were divided into normal group and Ang Ⅱ group.To investigate the effect of silencing BHLHE41(siBHLHE41)on cardiomyocyte hypertrophy and apoptosis,the cells were divided into 4groups:blank group[transfected with small in-terfering RNA(siRNA)+phosphate buffered saline(PBS)],siBHLHE41 group[transfected with siBHLHE41+PBS],model group(transfected with siRNA+Ang Ⅱ)and experimental group(transfected with siBHLHE41+Ang Ⅱ).The mRNA levels of BHLHE41,β-myosin heavy chain(β-MHC),atrial natriuretic peptide(ANP),B-type natriuretic peptide(BNP),poly ADP-ribose polymer-ase(PARP),B-cell lymphoma-2(Bcl-2),B-cell lymphoma-2-associated X protein(Bax),and p53 were detected by real-time fluorescence quantitative polymerase chain reaction(RT-qPCR).The protein expression levels of BHLHE41,Bax,Bcl-2,PARP and p53 were detected by Western blot.Phalloidin staining was used to observe the surface area of cardiomyocytes,TUNEL staining was used to observe cardiomyocytes apoptosis.Results Compared with the normal group,the mRNA and protein expression levels of BHL-HE41 was higher in the Ang Ⅱ group.Compared with blank group,the mRNA expression levels of β-MHC,ANP,BNP in the model group were upregulated,and the protein and mRNA expression levels of PARP,Bax and p53 in model group were significantly increased,the expression level of Bcl-2 was significantly decreased,the surface area of cardiomyocytes was significantly increased,and the apopto-sis rate of cardiomyocytes was significantly increased(P＜0.05).Compared with model group,the mRNA expression levels of β-MHC,ANP and BNP in the experimental group were upregulated,and the protein and mRNA expression levels of PARP,Bax and p53 in experi-mental group were significantly increased,the expression level of Bcl-2 was significantly decreased,the surface area of cardiomyocytes was increased,and the apoptosis rate of cardiomyocytes was significantly increased(P＜0.05).Conclusion Silencing BHLHE41 can aggravate Ang Ⅱ-induced hypertrophy and apoptosis of H9C2 cardiomyocytes,which may be related to the p53 activation of the apoptotic signaling pathway.

Objective To investigate the effect of YTH domain family protein 2(YTHDF2)on an-giotensin Ⅱ(Ang Ⅱ)-induced hypertrophy and apoptosis of primary neonatal rat cardiomyocytes.Methods The expression level of YTHDF2 was detected in the primary neonatal rat cardiomyo-cytes with or without Ang Ⅱ stimulation(AngⅡ group and normal group).The cells were divid-ed into blank group(transfected with siRNA+PBS),siYTHDF2 group(transfected with siYTHDF2+PBS),model group(siRNA+Ang Ⅱ)and experimental group(siYTHDF2+Ang Ⅱ)to investi-gate the effects of silencing YTHDF2 on the hypertrophy and apoptosis of cardiomyocytes.West-ern blotting and RT-qPCR were used to detect the expression of YTHDF2 at protein and mRNA levels,and RT-qPCR was employed to measure the mRNA levels of myocardial hypertrophic related genes atrial natriuretic peptide(ANP),brain natriuretic peptide(BNP)and beta-myosin heavy chain(β-MHC),and cardiomyocyte apoptosis related genes Bax and B lymphocytoma 2 gene(Bcl-2).The surface area of cardiomyocytes was observed by α-actin immunofluorescence staining.Cardiomyocyte apoptosis was observed by TUNEL staining,and the binding relationship between YTHDF2 and Bcl-2 was verified by immunoprecipitation.Results The expression of YTHDF2 at protein and mRNA levels were significantly higher in the AngⅡ group than the nor-mal group(1.49±0.03 vs 0.97±0.09,1.50±0.08 vs 1.00±0.07,P＜0.05).Compared with the blank group,the surface area of cardiomyocytes was notably enlarged,apoptotic rate was obvi-ously increased,the mRNA levels of ANP,BNP,β-MHC and Bax were significantly increased,and that of Bcl-2 was remarkably decreased in the model group(P＜0.05).The experimental group obtained decreased surface area and apoptotic rate of cardiomyocytes,lower mRNA levels of ANP,BNP,β-MHC and Bax,and increased mRNA expression of Bcl-2(P＜0.05).Conclusion Silencing YTHDF2 can alleviate Ang Ⅱ-induced hypertrophy and apoptosis in primary neonatal rat cardiomyocyte,and YTHDF2 inhibits the expression of Bcl-2 by binding to it.