Abstract: ObjectiveTo explore the mechanism of the miRNA455 delaying heart failure after longterm pressure load. MethodsFourweekold Kunming male mice were randomly divided into three groups， TAC mice with miR455(TAC.miR455) group， TAC mice with GFP(TAC.GFP) group， and sham operation mice with GFP(sham)group. TAC or sham operation was carried out. Hematoxylin and eosin(HE) and Masson staining were carried out on the myocardial tissue to observe the histopathological changes in mice after four weeks of operation. Western blot was applied to detect apoptosis protein. qRTPCR and Western blot were applied to detect miR455 target genes and proteins. ResultsSignificant increase of miR455 gene in the miR455treated hearts of TAC were observed（P<0.01）. Myocardial collagen fibers and cell apoptosis were significantly reduced in the miR455treated hearts of TAC(P<0.05). Western blot  showed that Calr was one of the target proteins in miR – 455. PCR results dedicated that Clar decreased with calr mRNA.ConclusionmiR455 attenuates the progressive deterioration of left ventricular function. The mechanism is that ventricular remodeling is improved by Calr falling through  miR455  making target mRNA degradation.

Key words: heart failure,conjestive, miR455;calreticulin