ASSA13-03-3 The Research For Molecular Mechanism of miR-93 Negative Regulation on Stat3 Transduction Pathway in Cardiac Hypertrophy. (29th April 2013)

• Record Type: Journal Article
• Authors: Mei, Tang; Min, Li; Cuiying, Wang; Yingshuo, Huang; Liling, Wu
• Is Part Of: Heart. Volume 99(2013)Supplement 1
• Page Start: A14
• Page End: A15
• Publication Date: 2013-04-29
• Subjects: Heart -- Diseases -- Treatment -- Periodicals; Cardiology -- Periodicals; 616.12
• DOI: 10.1136/heartjnl-2013-303992.043
• Languages: English
• ISSNs: 1355-6037

Abstract

Abstract : Objective: The purpose of this research was to investigate the role of miR-93 in cardiac hypertrophy and its relation with Stat3 signal transduction pathway in vitro. To identify the effect of miR-93 involved Stat3 pathway on cardiac hypertrophy cells. Methods: The cultured neonatal rat cardiomyocyte was used to observe the hypertrophic effect of phenephrine, and the hypertrophic response was assayed bymeasuring the cell diameter, protein content and miR-93 expression. The experiment of double luciferase report gene was used to elucidate interaction between miR-93 and stat3. The expression of brain natriuretic peptide (BNP), atrial natriuretic factor (ANF) and Stat3 were measured by western blot. Results: In cultured cardiomyocytes, PE induced profound hypertrophic morphology change and the significant increase in cell diameter, and protein content in a concentration - dependentmanner compared with those in vehicle control (P < 0.01). The contradictory result was found in cardiomyocytes transfected with miR-93 (P < 0.01). miR-93 at concentration of 10 –7 mol/L significantly inhibited ANF and BNP expressions and the protein expressions of Stat3 compared with those in the vehicle control (P < 0.001). Interaction between miR-93 and Stat3 exists through uciferase report gene experiment. miR-93 markedly inhibited the myocyte hypertrophy (P < 0.01). Conclusions: Cardiomyocyte hypertrophy induced by PE may be, at least in part, mediated by Stat3 signal transduction pathway inhibited by increasing miR-93. Our results show that miR-93 may play a critical role as therapy factor in the Cardiomyocyte hypertrophy. This work was supported by Beijing Natural Science Foundation (7112033).