[Association between wnt signal pathway and post-infarction cardiac remodeling/rupture in aged mice]

Zhonghua Xin Xue Guan Bing Za Zhi. 2009 Sep;37(9):826-31.
[Article in Chinese]

Abstract

Objective: To observe the association between wnt signal pathway and post infarction left ventricular remodeling/rupture in mice with various ages.

Methods: Three months-old (young group, n = 116) and 18 months-old (aged group, n = 116) male C57/BL mice were studied. Seventy mice underwent ligation of left coronary artery, 10 sham-operation and echocardiography and hemodynamics were performed 7 d post-infarction, 36 infarcted mice were used for detecting expression of dvl-1, beta-catenin and connexin 43 in left ventricular (LV) myocardium and infarction region at 3 d, 7 d, 14 d post infarction (n = 12 each).

Results: Incidence of cardiac rupture was significantly higher in aged mice than in young mice (36.7% vs. 16.7%, P < 0.05) and degree of LV dilation and contractile dysfunction was significantly severer in aged mice than those in young mice post infarction. Expression of dvl-1, beta-catenin in left ventricle was upregulated in MI group compared with sham group (P < 0.05), expression of dvl-1 and beta-catenin in infarction region in MI 3d group in aged mice was significantly downregulated than in young mice (P < 0.05). Expression of connexin 43 is 2.15 fold higher in young sham mice than in aged sham mice (P < 0.05) and decreased significantly post infarction (P < 0.05). Expression of connexin 43 in infarction region in mice 3 d and 14 d post infarction was significantly lower in aged mice than in respective young mice (all P < 0.05).

Conclusion: Reductant activation of wnt signal pathway post infarction in aged mice might be responsible for increased incidence of cardiac rupture and aggravated remodeling.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aging
  • Animals
  • Heart Rupture / etiology*
  • Heart Ventricles
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Myocardial Infarction / metabolism*
  • Myocardial Infarction / pathology*
  • Myocardium / metabolism*
  • Signal Transduction*
  • Ventricular Remodeling
  • Wnt Proteins / metabolism

Substances

  • Wnt Proteins