title: [Relationship between myocardial microRNA-30a expression and myocardial fibrosis in rats post myocardial infarction].
abstract: OBJECTIVE
  To explore the potential role and mechanism of microRNA(miR)-30a in myocardial fibrosis after myocardial infarction (MI).
  
  
  METHODS
  Rats were randomly divided into 1 week MI group (n=11), 2 weeks MI group (n=13) and 4 weeks MI group (n=15) by applying random number table after left anterior descending coronary artery ligation. Rats in Sham group were examined at respective time points (n=16). Heart function was monitored by echocardiography. Myocardial collagen volume fraction (CVF) was determined on Masson stained sections. Myocardial expression of collagen Ⅰ and Ⅲ was determined by immunohistochemistry. The myocardial mRNA level of miR-30a, TGF-β1 and CTGF were detected by real time-quantitative PCR analysis. The myocardial protein levels of TGF-β1 and CTGF were measured by Western blot analysis.
  
  
  RESULTS
  The LVEDD ((8.37±0.58) mm) and LVESD ((6.12±0.82) mm) in 4 weeks MI group were significantly higher than those in Sham group ((6.08±0.57) mm, (4.17±0.60) mm), all P<0.01. The FS ((27.0±3.9) %) and LVEF ((51.0±6.3) %) in 4 weeks MI group were significantly lower than those in Sham group ((47.0±2.1) %, (82.0±2.3)%), all P<0.01. The level of myocardial CVF in 1 week MI group, 2 weeks MI group and 4 weeks MI group were significantly higher than in Sham group (all P<0.01) in a time-dependent manner. The level of myocardial collagen Ⅰ and Ⅲ was increased gradually from 1 week to 4 weeks post MI compared with Sham group (all P<0.01). The collagen Ⅰ/Ⅲ ratio was similar between 1 week MI group and Sham group (P=0.58), however, which was significantly higher in 2 weeks MI group and 4 weeks MI group compared with Sham group (all P<0.01), and the ratio was significantly higher in 4 weeks MI group than 2 weeks MI group (P<0.01). The level of miR-30a was significantly and gradually reduced in all MI groups compared with Sham group (all P<0.01). The mRNA and protein levels of TGF-β1 and CTGF were significantly and gradually increased after MI compared with Sham group (all P<0.001).
  
  
  CONCLUSIONS
  Our results indicate that overexpression of miR-30a after MI might be a potential strategy for suppressing myocardial fibrosis by modulating the mRNA and protein levels of TGF-β1 and CTGF.
authors.affiliation: Department of Cardiology, Nanjing Hospital Affiliated to Nanjing Medical University, Nanjing 210006, China.
authors.forename: L W
authors.initials: LW
authors.lastname: Chen
authors.forename: L L
authors.initials: LL
authors.lastname: Zhu
authors.forename: Q
authors.initials: Q
authors.lastname: Ji
authors.forename: H
authors.initials: H
authors.lastname: Zhu
authors.forename: Y Z
authors.initials: YZ
authors.lastname: Ren
authors.forename: Z G
authors.initials: ZG
authors.lastname: Fan
authors.forename: X B
authors.initials: XB
authors.lastname: Li
authors.forename: X F
authors.initials: XF
authors.lastname: Gao
authors.forename: Y J
authors.initials: YJ
authors.lastname: Zhang
authors.forename: N L
authors.initials: NL
authors.lastname: Tian
mesh_terms: D000818:Animals; D009202:Cardiomyopathies; D024042:Collagen Type I / Q000378:metabolism; D024061:Collagen Type III / Q000378:metabolism; D055513:Connective Tissue Growth Factor / Q000378:metabolism; D004452:Echocardiography; D035683:MicroRNAs / Q000378:metabolism*; D009203:Myocardial Infarction / Q000378:metabolism* / Q000473:pathology; D009206:Myocardium / Q000473:pathology*; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D053773:Transforming Growth Factor beta1 / Q000378:metabolism
chemical_list: C526316:CCN2 protein, rat; D024042:Collagen Type I; D024061:Collagen Type III; C556157:MIRN30 microRNA, rat; D035683:MicroRNAs; D012333:RNA, Messenger; C508962:Tgfb1 protein, rat; D053773:Transforming Growth Factor beta1; D055513:Connective Tissue Growth Factor