Role of PARP-2 selective inhibitor in cardiac hypertrophy in neonatal rat cardiomyocytes
Geng Bia
Abstract
Geng Bia
Abstract
Objective: To explore the effects of PARP-2 on the cardiac hypertrophy in vitro. Methods: The expression of PARP-2was knocked down by using selective inhibitor UPF1069 in neonatal rat cardiomyocytes and the cardiomyocyte hypertrophy was evaluated by measuring the mRNA levels of ANF,BNP,and β-MHC and cell-surface area. Results:In the neonatal rat cardiomyocytes,the expression of PARP-2 knocked down by using selective inhibitor UPF1069,indicating that endogenous PARP-2 played a positive regulatory role in cardiac hypertrophy. Conclusion: Knockdown of PARP-2 protects cardiomyocytes from hypertrophy.
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
Objective: To explore the effects of PARP-2 on the cardiac hypertrophy in vitro. Methods: The expression of PARP-2was knocked down by using selective inhibitor UPF1069 in neonatal rat cardiomyocytes and the cardiomyocyte hypertrophy was evaluated by measuring the mRNA levels of ANF,BNP,and β-MHC and cell-surface area. Results:In the neonatal rat cardiomyocytes,the expression of PARP-2 knocked down by using selective inhibitor UPF1069,indicating that endogenous PARP-2 played a positive regulatory role in cardiac hypertrophy. Conclusion: Knockdown of PARP-2 protects cardiomyocytes from hypertrophy.
Key concepts: Gene knockdown, Poly ADP ribose polymerase, Muscle hypertrophy, Endogeny, PARP inhibitor, Myocyte, Internal medicine, Endocrinology