title: [Inhibition of microRNA195 attenuates high-glucose induced neonatal cardiomyocytes hypertrophy in vitro].
abstract: OBJECTIVE
  To investigate the effects of micro(mi) RNA-195 on high-glucose induced neonatal cardiomyocyte hypertrophy and to explore the related mechanism.
  
  
  METHODS
  The potential target gene of miRNA-195 (Smad7) was predicted by TargetScan5. 1 software. Cardiomyocytes were isolated from neonatal SD rats and cells were then randomly divided into three groups: cells treated by culture medium containing 5 mmol/L glucose (control group) , by culture medium containing 25 mmol/L glucose (high glucose group) and treated by culture medium containing 25 mmol/L glucose and miRNA-195 inhibitor transfection (miRNA-195 inhibitor group). After 24, 48, or 72 h of in vitro culture, the morphology of cardiomyocytes was examined under phase contrast microscope. Micrographs were captured and the cell surface was calculated. The mRNA expressions of miRNA-195 and myosin heavy chain β (β-MHC), a biomarker for cardiomyocyte hypertrophy, in cardiomyocytes were detected by RT-PCR. The protein expression of Smad7 was determined by Western blot. The concentration of transforming growth factor-β1 (TGF-β1) in the supernatant of culture medium was measured by ELISA.
  
  
  RESULTS
  Cross-sectional area of cardiomyocytes, expression of miRNA-195 and β-MHC and secretion of TGF-β1 were significantly increased in high glucose-treated cells (P < 0.05 vs. normal control). The protein expression of Smad7 was significantly downregulated in cells exposed to high glucose for 48 h (P < 0.05 vs. normal control). Downregulation of miRNA-195 partly reversed the high glucose-induced effects. The expression of Smad7 was negatively correlated with miRNA-195 in high glucose control group (correlation coefficient: -0.945, P < 0.05).
  
  
  CONCLUSIONS
  Our results demonstrate that Smad7 could be the target gene of miRNA-195. miRNA-195 might play a crucial role in the development and progression of diabetic cardiomyopathy possibly through downregulating the expression of Smad7 and modulating TGF-β/Smad pathways.
authors.forename: Kong
authors.initials: K
authors.lastname: Biao
authors.forename: Shen
authors.initials: S
authors.lastname: Dongli
authors.forename: Rui
authors.initials: R
authors.lastname: Tao
authors.forename: Zhang
authors.initials: Z
authors.lastname: Guohui
mesh_terms: D000818:Animals; D015536:Down-Regulation; D005947:Glucose; D006984:Hypertrophy; D035683:MicroRNAs; D032383:Myocytes, Cardiac; D051381:Rats; D017207:Rats, Sprague-Dawley; D014162:Transfection; D053773:Transforming Growth Factor beta1
chemical_list: D035683:MicroRNAs; D053773:Transforming Growth Factor beta1; D005947:Glucose