Objective      To investigate the alteration of miR-199a-5p expression in cardiomyocyte hypertrophy induced by angiotensin Ⅱ (AngⅡ).       Methods      The rat model of cardiac hypertrophy was established by transverse aortic coarctation. Thirty SD rats were randomly divided into 3 groups

sham

group

model group

and losartan group (n=10 for each group). The losartan group was injected intraperitoneally with losartan potassium 10 mg/(kg·d). The sham group and model group were treated with the vehicle. On day 28

the cardiac mass index (CMI) and left ventricular mass index (LVMI) were measured. The myocardial tissue morphologic changes were detected by hematoxylin-eosin staining. Quantitative RT-PCR was performed to analyze the expression level of miR-199a-5p. Neonatal rat cardiac myocytes treated by AngⅡ were exposed to losartan

and miR-199a-5p expression level was detected by quantitative RT-PCR. MiR-199a-5p mimic and inhibitor were used to transfect neonatal rat cardiac myocytes

and cardiomyocyte hypertrophy was assessed by [

3

H

]

-leucine incorporation.       Results      The cardiac myocytes were hypertrophic and the expression level of miR-199a-5p was significantly increased in left ventricle induced by transverse aortic coarctation (

P

0.05). AngⅡ  receptor antagonist losartan significantly reversed the changes. Losartan significantly decreased the expression level of miR-199a-5p in neonatal rat cardiac myocytes induced by AngⅡ (

P

0.05). MiR-199a-5p inhibitor significantly decreased [

3

H

]

-leucine incorporation in neonatal rat cardiac myocytes induced by AngⅡ (

P

0.01)

while miR-199a-5p mimic significantly enhanced the incorporation (

P

0.01).       Conclusion      MiR-199a-5p is an important regulator in myocyte hypertrophy induced by AngⅡ

and may play a significant role in myocyte hypertrophy signaling pathways induced by AngⅡ.