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- W3141926229 abstract "Cardiac hypertrophy is an adaptive process to an increased hemodynamic overload.However,the adaption may lead to the fragility of myocardium facing pathological stimuli.In the present study,experiments were designed to explore the susceptibility of hypertrophic myocardiocytes to apoptotic stimuli and the role of protein kinase Cδ(PKCδ) during the transition from hypertrophy to apoptosis.Endothelin-1 (ET-1)-treated cardiomyocytes were used as model of cardiac hypertrophy.AngiotensinⅡ(AngⅡ) was used as an apoptotic stimulus.Cell surface area was measured to determine the extent of hypertrophy.The apoptotic rate in cardiomyocytes was detected by Hoechst 33258.(1) Cell surface area was increased by 42.5% and 67.3% following 1 nmol/L and 10 nmol/L ET-1 treatment,respectively,as compared with serum-free cultured myocytes.So the mildly and moderately hypertrophic myocyte models were set up.(2) Apoptotic rates in serum-free cultured,mildly and moderately hypertrophic myocytes after AngⅡtreatment were (15.54±1.32)%,(20.65±1.40)% and (29.33±3.52)%,respectively.It is suggested that hypertrophic myocytes are more susceptive to apoptotic stimulus.(3) Rottlerin,a specific inhibitor of PKCδdepressed apoptotic rates induced by AngⅡto (15.88±2.25)% in mildly hypertrophic myocytes and to (15.01±1.37)% in moderately hypertrophic myocytes;but rottlerin did not affect apoptotic rate induced by AngⅡin serum-free cultured myocytes.These results suggest that inhibition of PKCδcan reduce Ang 11-induced apoptosis of hypertrophic cardiomyocytes and that PKCδis possibly involved in the apoptotic process of hypertrophic cardiomyocytes." @default.
- W3141926229 created "2021-04-13" @default.
- W3141926229 creator A5010374786 @default.
- W3141926229 date "2006-01-01" @default.
- W3141926229 modified "2023-09-27" @default.
- W3141926229 title "Protein kinase Cδis possibly involved in the transition from hypertrophy to apoptosis of myocardiocytes" @default.
- W3141926229 hasPublicationYear "2006" @default.
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