Yuan-yuan Fan, B. Long, Fang Liu, Luyu Zhou, Kun Wang, Peifeng Li
{"title":"Establishment of Cardiomyocyte-specific miR-30b Transgenic Mice and Exploring The Function of miR-30b","authors":"Yuan-yuan Fan, B. Long, Fang Liu, Luyu Zhou, Kun Wang, Peifeng Li","doi":"10.3724/SP.J.1206.2013.00206","DOIUrl":null,"url":null,"abstract":"MicroRNAs(miRNAs) array results have shown that the expression of miR-30b is downregulated in heart tissues from patients with familial hypertrophic cardiomyopathy who were carriers of missense mutations in the MYH7,and also in a murine heart failure model,implying that miR-30b might play an important role in heart diseases.To study miR-30b in vivo function,we generated a transgenic mouse line overexpressing miR-30b under the control of the 5.5 kb promoter of α-myosin heavy chain(α-MHC).qRT-PCR results demonstrated that miR-30b was significantly increased in the heart tissues of miR-30b transgenic mice(P 0.05).miR-30b transgenic mice did not exhibit significant heart/body weight and left ventricular(LV)/body weight changes and abnormal myocardium structure.At present,little is known about how miR-30b regulates myocardial infarction.We constructed I/R models by the coronary artery ligation method and sham-operated mice were used as controls.Biochemical detection results and TTC-Evans blue results showed that after ischemia-reperfusion,these transgenic mice had lower releases of LDH,CK and cTn玉(P 0.05)and their hearts exhibited a smaller infarct size compared to those from control mice(P 0.05).Echocardiographic results indicated that cardiac function of transgenic mice was markedly improved compared to that of control mice.In conclusion,miR-30b has protective effect upon ischemic-reperfusion injury.And it may provide a new therapeutic approach for preventing and treating myocardial infarction.","PeriodicalId":0,"journal":{"name":"","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.3724/SP.J.1206.2013.00206","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
Abstract
MicroRNAs(miRNAs) array results have shown that the expression of miR-30b is downregulated in heart tissues from patients with familial hypertrophic cardiomyopathy who were carriers of missense mutations in the MYH7,and also in a murine heart failure model,implying that miR-30b might play an important role in heart diseases.To study miR-30b in vivo function,we generated a transgenic mouse line overexpressing miR-30b under the control of the 5.5 kb promoter of α-myosin heavy chain(α-MHC).qRT-PCR results demonstrated that miR-30b was significantly increased in the heart tissues of miR-30b transgenic mice(P 0.05).miR-30b transgenic mice did not exhibit significant heart/body weight and left ventricular(LV)/body weight changes and abnormal myocardium structure.At present,little is known about how miR-30b regulates myocardial infarction.We constructed I/R models by the coronary artery ligation method and sham-operated mice were used as controls.Biochemical detection results and TTC-Evans blue results showed that after ischemia-reperfusion,these transgenic mice had lower releases of LDH,CK and cTn玉(P 0.05)and their hearts exhibited a smaller infarct size compared to those from control mice(P 0.05).Echocardiographic results indicated that cardiac function of transgenic mice was markedly improved compared to that of control mice.In conclusion,miR-30b has protective effect upon ischemic-reperfusion injury.And it may provide a new therapeutic approach for preventing and treating myocardial infarction.