MicroRNA-133a improves the cardiac function and fibrosis through inhibiting Akt in heart failure rats - 08/05/15
, Zheng-Ming Jiang a, Qiu-Ping Zhao b, Fu Xin aBienvenue sur EM-consulte, la référence des professionnels de santé.
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Abstract |
Objective |
MicroRNAs (miRNAs), a group of small non-coding RNAs that fine tune translation of multiple target mRNAs, have been implicated in the development and progression of heart failure.
Methods |
The present study was undertaken to determine the roles of miR-133a on the anatomical, hemodynamic and fibrosis of heart in the chronic heart failure rats, and the downstream signaling pathway.
Results |
The expression of miR-133a in the heart of chronic heart failure from patients or rats was decreased. The miR-133a mimic and miR-133a overexpression caused a decrease in the heart weight/body weight (HW/BW) and LVEDP, and an increase in the LVSP and +LV dP/dtmax in the chronic heart failure rats. However, the miR-133a inhibitor promoted the HW/BW and LVEDP, and caused a decrease in the LVSP and LV dP/dtmax in the chronic heart failure rats. The miR-133a mimic and miR-133a overexpression significantly caused a decrease in the fibrosis of heart in chronic heart failure rats. The Akt inhibitor TCN abolished the effects of miR-133a on the HW/BW and LVEDP decrease, LVSP and LV dP/dtmax increase in the chronic heart failure rats. The miR-133a increased the expression of phosphorylated Akt in the heart of chronic heart failure rats.
Conclusion |
These results demonstrated that miR-133a improves the cardiac function and fibrosis through inhibiting Akt in heart failure rats.
Le texte complet de cet article est disponible en PDF.Keywords : miR-133a, Fibrosis, Akt, Heart failure
Plan
Vol 71
P. 185-189 - avril 2015 Retour au numéro
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