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摘要
Background Left ventricular(LV) remodeling is the most common target organ damage in hypertension.Previously,our study found that plasma micro RNA-29a(miR-29a) level was associated with the LV remodeling in hypertensive patients.However,the causal relationship between miR-29a and LV remodeling remains unknown.Thus,the aim of this study was to investigate the regulation mechanism of mi R-29a in LV remodeling.Methods & Results Overexpression and knockdown miR-29a mice were generated by tail-intravenous injection of mi R-29 a-mimic and inhibitor lentivirus for one week respectively.Then the mice were subjected to angiotensin-II(Ang II) induced LV remodeling by subcutaneous Ang II capsule osmotic pumping into Ang II for four weeks.Ang II-induced LV remodeling mice as the model group(n = 9).Age-matched male SPF C57/BL6J mice(6–8 weeks old) were treated with the pumping of saline as a vehicle(n = 6).In vivo,overexpression miR-29a ameliorated Ang II-induced LV remodeling,while knockdown miR-29a deteriorated LV remodeling.Simultaneously,we observed that overexpression miR-29a mice inhibited but knockdown miR-29a mice increased cardiac cross-sectional area,indicating that mi R-29 a has an antagonistic effect on cardiac hypertrophy.Further studies found that overexpression miR-29a inhibited the content of the LV collagen including collagen I and III.Moreover,the expression of transforming growth factor-β(TGF-β) and phosphorylated SMAD2/3 decreased with the down-regulation of collagen I and III in overexpression mi R-29a mice.Conclusions Our finding indicates that overexpression miR-29a attenuates LV remodeling by inhibiting collagen deposition,TGF-β,and phosphorylated SMAD2/3 expression.Thus,intervention miR-29a may be a therapeutic target for attenuating LV remodeling.
