Objective:Myocardial infarction(MI)remains the leading cause of morbidity and mortality due partly to the limited regenerative capacity of cardiomyocytes to replace cardiomyocyte lost due to apoptosis.Inhibiting cardi...Objective:Myocardial infarction(MI)remains the leading cause of morbidity and mortality due partly to the limited regenerative capacity of cardiomyocytes to replace cardiomyocyte lost due to apoptosis.Inhibiting cardiomyocyte apoptosis is recognized as an effective therapeutic approach for MI.MicroRNAs(miRNAs,miRs),which regulate target genes at the post-transcriptional level,play a significant role in the regulation of cardiovascular diseases such as MI.MicroRNA-135b(miR-135b)has a protective effect on cardiomyocytes.However,the role of miR-135b in cardiomyocyte apoptosis in infarct myocardium needs further clarification.Methods:We generatedα-MHC-miR-135b transgenic mice to investigate the role of miR-135b in myocardial injury after MI.MiR-135b mimic and negative control(NC)were transfected into H2O2-induced cardiomyocytes to evaluate the effect of overexpression of miR-135b on the levels of reactive oxygen species(ROS)and apoptosis.Results:Our results showed that overexpression of miR-135b had protective effect on cardiomyocyte injury both in vivo and in vitro.MiR-135b inhibited cardiomyocyte apoptosis and ROS generation,downregulated pro-apoptosis proteins(cleaved-caspase-3 and Bax),and increased anti-apoptosis protein(Bcl-2).Moreover,miR-135b showed an inhibitory effect on apoptosis-related protein target transient receptor potential vanilloid-type 4(TRPV4)cation channel.Conclusion:MiR-135b might be considered a new molecular target for potential replacement therapy as antiapoptotic cardioprotection in the setting of MI.展开更多
目的研究miR-21在弥漫大B细胞淋巴瘤(diffuse large B-cell lymphoma,DLBCL)中的表达,探讨miR-21表达与DL-BCL临床病理特征的关系及其在DLBCL发生发展中的意义。方法采用Real-time RT-PCR方法检测36例DLBCL和10例正常淋巴结中miR-21的表...目的研究miR-21在弥漫大B细胞淋巴瘤(diffuse large B-cell lymphoma,DLBCL)中的表达,探讨miR-21表达与DL-BCL临床病理特征的关系及其在DLBCL发生发展中的意义。方法采用Real-time RT-PCR方法检测36例DLBCL和10例正常淋巴结中miR-21的表达,并采用免疫组织化学SP法检测Ki-67、PTEN在DLBCL中的表达。结果miR-21在DLBCL中高表达,36例DLBCL中有14例表达PTEN(38.9%),21例Ki-67≥50%(58.3%)。DLBCL中miR-21表达水平与PTEN蛋白表达呈负相关,其高表达与DLBCL高Ann Arbor分期、高增殖指数(Ki-67≥50%)、国际预后指数(IPI)呈正相关。结论miR-21过表达可能是DLBCL恶性度高的标志,是促进DLBCL肿瘤细胞增殖的重要因素。PTEN可能是miR-21在DLBCL发挥作用的靶标。展开更多
基金supported by CAMS Innovation Fund for Medical Sciences of China(2019-I2M-5-078)National Natural Science Foundation of China(Grant No.81861128022)Natural Science Foundation of Heilongjiang Province(Grant No.LH2019H003).
文摘Objective:Myocardial infarction(MI)remains the leading cause of morbidity and mortality due partly to the limited regenerative capacity of cardiomyocytes to replace cardiomyocyte lost due to apoptosis.Inhibiting cardiomyocyte apoptosis is recognized as an effective therapeutic approach for MI.MicroRNAs(miRNAs,miRs),which regulate target genes at the post-transcriptional level,play a significant role in the regulation of cardiovascular diseases such as MI.MicroRNA-135b(miR-135b)has a protective effect on cardiomyocytes.However,the role of miR-135b in cardiomyocyte apoptosis in infarct myocardium needs further clarification.Methods:We generatedα-MHC-miR-135b transgenic mice to investigate the role of miR-135b in myocardial injury after MI.MiR-135b mimic and negative control(NC)were transfected into H2O2-induced cardiomyocytes to evaluate the effect of overexpression of miR-135b on the levels of reactive oxygen species(ROS)and apoptosis.Results:Our results showed that overexpression of miR-135b had protective effect on cardiomyocyte injury both in vivo and in vitro.MiR-135b inhibited cardiomyocyte apoptosis and ROS generation,downregulated pro-apoptosis proteins(cleaved-caspase-3 and Bax),and increased anti-apoptosis protein(Bcl-2).Moreover,miR-135b showed an inhibitory effect on apoptosis-related protein target transient receptor potential vanilloid-type 4(TRPV4)cation channel.Conclusion:MiR-135b might be considered a new molecular target for potential replacement therapy as antiapoptotic cardioprotection in the setting of MI.
