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ASSA13-03-3 The Research For Molecular Mechanism of miR-93 Negative Regulation on Stat3 Transduction Pathway in Cardiac Hypertrophy
  1. Tang Mei,
  2. Li Min,
  3. Wang Cuiying,
  4. Huang Yingshuo,
  5. Wu Liling
  1. Department of General medicine. Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China

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).

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