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Insulin-like growth factor-1 protecting cardiomyocytes from apoptosis by down-regulating transcription factor basic transcription element binding protein through extracellular regulated kinase 1 /2 pathway
Pages: 329-335
Year: Issue:  3
Journal: Acta Anatomica Sinica

Keyword:  CardiomyocyteInsulin-like growth factor-1Basic transcription element binding proteinExtracellular regulated kinase1 /2Western blottingRat;
Abstract: Objective To investigate gene regulation mechanism of insulin-like growth factor-1( IGF-1) antiapoptotic effect on rat cardiomyocytes. Methods Primary neonatal rat cardiomyocytes( NRCMs) were cultured in vitro,IGF-1( 10 nmol / L) was added with different signal transduction pathway inhibitors [phosphatidylinositol 3-kinase( PI3K),extracellular regulated kinase( ERK) 1 /2 and Raf-1]respectively( 20μmol / L). The gene expression of basic transcription element binding protein( BTEB) was detected by RT-PCR and Western blotting,by which the pathway of IGF-1 downregulated BTEB gene expression was judged. NRCMs were treated with 100 umol / L hydrogen peroxide( H2O2) to induce apoptosis. BTEB specific siRNA was transfected into the cells by Lipofectamine 2000. Myocardial cells apoptosis was detected by DNA-ladder analysis,Annexin V-FITC / PI dual staining,Caspase-3 activity assay and Hoechst33258 staining.Results The mRNA and protein expression levels of BTEB gene in NRCMs were down-regulated significantly after IGF-1had stimulated for 60 minutes. Compared with control groups,BTEB mRNA and protein expression in ERK1 /2 pathway inhibitor PD98059 group was significantly higher( P < 0. 01). The apoptosis of NRCMs was induced by H2O2. Artificiallyinhibited BTEB gene expression with BTEB specific siRNA,BTEB mRNA and protein expression decreased obviously( P <0. 05). Compared with control group,the apoptotic rates of NRCMs induced by H2O2 in IGF-1 group and BTEB specific siRNA groups were declined( all P < 0. 05),decreased Caspase-3 activity( all P < 0. 05),attenuated DNA fragmentation and reduced apoptotic bodies were also observed in these groups. The anti-apoptotic effect of BTEB gene silencing on NRCMs was similar with that of IGF-1 treatment. Conclusion IGF-1 protects cardiomyocytes from apoptosis by downregulating transcription factor BTEB through ERK1 /2 pathway.
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