| Objective: Cardiovascular disease has the highest mortality in theworld.Acute myocardial infarction(AMI) result in ventricular remodelingwhich makes cardio function worse and leads to heart failure. Research-ers have found that several miRNAs have aberrant expression in impair-ed cardiomyocytes, it suggest that these miRNAs may play an importantrole during the process of cardiomyocytes injury. We have found thatmiR-214expression aberrantly in AMI rat cardiomyocyts, and researcherhas been demonstrated that miR-214play an positive role in mice A-MI. To demonstrated microRNA-214(miR-214) expression was upregulat-ed in AMI rat model.Overexpression miR-214was benefit to LV remod-eling which improved the heart’s systolic and diastolic function in AMIrat,which knockdown miR-214make heart function worse. The mechan-ism is related though Phosphatase and Tensin Homolog(PTEN) inhibition.Methords:The total of120AMI rats which made by ligating the l-eft anterior descending were divided into ten groups:a group:sham group(n=16),b group: AMI group (n=24), c group: ad-miR-214group (n=8),d group: anti-miR-214group(n=8),e group:ad-GFP group(n=16),f group:ad-miR-214with AMI group(n=16),g group:anti-miR-214with AMI gro-up(n=16),h group: ad-GFP with AMI group(n=8),i group:ad-miR-214andanti-PTEN with AMI group(n=8),j group:anti-miR-214and anti-PTENwith AMI group(n=8).To detect the index which can reflect the left ven-tricular remodeling in f,g and h group at8weeks, compared the differ-ences among groups;to detect miR-214expression in infarcted,border andnon-infarcted areas of b group at6h,12h and24h after AMI,comparedthe differences among the time course in the same areas, respectively;to detect PTEN expression in b group at24h,c group, group d group ande group at4days,compared the differences among groups;to detect cellapoptosis in inarcted and border areas of a,f,g,h,i,and j groups at24h,compared the differences among groups in the same areas.Results:Compared with non-infarcted areas, at6h,13h and24h afterAMI,miR-214was upregulated in both border and infarcted areas,in in-farcted area,miR-214expression was2.88times,2.35times and1.98ti-mes more than non-infarcted areas at6h,12h and24h,respectively(P<0.05);in border areas, miR-214expression was1.36times,1.79times and2.28times more than non-infarcted areas at6h,12h and24h,respectively(P<0.05); compared with h group at8weeks, heart rate(HR) decreased7.94%, left ventricular end-diastolic pressure (LVEDP) was decreased41.01%,left ventricular/body weight(LV/BW) was decreased8.16%, infarc-ted area size was decreased14.4%and left ventricular diameter was d-ecreased16.98%, left ventricular systolic pressure(LVSP) was increased32.70%,the first derivatives (positive and negative) of LV pressure overtime(±dp/dt) were increased32.4%and36.07%in f group at8weeks,HR was increased8.67%,LVEDP was increased43.23%, LV/BW was i-ncreased6.94%,infarcted area size was increased8.2%and left ventricu-l-ar diameter was increased22.98%,LVSP was decreased11.31%,±dp/dtwere decreased14.73%and19.67%in g group at8weeks,respectively,(P<0.05); compared tieh h group at24h,cell apoptosis was decreased bo-th in infarcted and border areas in f group at24h,and increased bothin infarcted and border areas in g group at24h,but there were no diffe-rences between I and j group at24h both in infarcted and border areas,respectively,there were also no differences among h,i and j group at24hboth in infarcted and border areas,respectively; compared with e groupat4days,PTEN expression was decreased in c group at4days, borderand infarcted areas in b group at24h, and increased in d group at4d-ays.Conclusion: MiR-214expression was upregulated in AMI rat model. Overexpression miR-214was benefit to LV remodeling which improvedthe heart’s systolic and diastolic function in AMI rat,which knockdownmiR-214make heart function worse.The mechanism is related though P-hosphatase and Tensin Homolog(PTEN) inhibition. |
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