OBJECTIVE: To determine the role of microRNA 21(miR-21) on left ventricular 
remodeling of rat heart with ischemia-reperfusion (I/R) injury and to 
investigate the underlying mechanism of miR-21 mediated myocardium protection.
METHODS: Rats were randomly divided into three groups: an I/R model group with 
Ad-GFP (Ad-GFP group), an I/R model group with Ad-miR-21 (Ad-miR-21 group) and a 
sham-surgery group. Changes in hemodynamic parameters were recorded at 1 week 
after I/R. Histological diagnosis was achieved by hematoxylin and eosin (H&E). 
Left ventricular (LV) dimensions, myocardial infarct size, LV/BW, collagen type 
Ⅰ, type Ⅲ and PCNA positive cells were measured. Primary cultures of neonatal 
rat cardiac ventricular myocytes were performed and cell ischemic injury was 
induced by hypoxia in a serum- and glucose-free medium, and reoxygenation (H/R). 
MiR-21 inhibitor and pre-miR-21 were respectively added to the culture medium 
for the miR-21 knockdown and for the miR-21 up-regulation. qRT-PCR was used to 
determine the miR-21 levels in cultured cells. Flow cytometry was performed to 
examine the cell apoptosis.
RESULTS: In the Ad-miR-21 group, LV dimensions, myocardial infarct size, LV/BW, 
collagen type Ⅰ, type Ⅲ and PCNA positive cells all significantly decreased 
compared with the Ad-GFP group. At 1 week after I/R, the Ad-miR-21 significantly 
improved LVSP, LV +dp/dt(max), LV - dp/dt(min), and decreased heart rate (HR) 
and LVEDP compared with the Ad-GFP group. Compared with the Ad-GFP, the cell 
apoptotic rate significantly decreased in the Ad-miR-21 group. The miR-21 
inhibitor exacerbated cardiac myocyte apoptosis and the pre-miR-21 decreased 
hypoxia/reoxygenation- induced cardiac myocyte apoptosis.
CONCLUSIONS: Ad-miR-21 improves LV remodeling and decreases the apoptosis of 
myocardial cells, suggesting the possible mechanism by which Ad-miR-21 functions 
in protecting against I/R injury.