[Changes of ErbB receptors mRNA expression in left ventricle of myocardial infarction]

Zhejiang Da Xue Xue Bao Yi Xue Ban. 2008 Jul;37(4):381-5. doi: 10.3785/j.issn.1008-9292.2008.04.010.
[Article in Chinese]

Abstract

Objective: To investigate the changes of ErbB receptors mRNA expression in left ventricle of myocardial infarction and its mechanism.

Methods: Myocardial infarction was induced by ligation of the left anterior descending coronary artery in male Sprague Dawley(SD) rats. After 1 month, the rats were sacrificed and mRNA was extracted from the left ventricle. mRNA was also extracted from ventricular myocytes of neonatal SD rats which were cultured under serum deprivation and hypoxia for 5 d. Expression of ErbB receptors mRNA were detected by real-time quantitative PCR.

Result: The mRNA expression of ErbB2 and ErbB4 receptors was significantly down-regulated in the left ventricle of myocardial infarction compared with the normal left ventricle; in contrast, there were no changes in mRNA expression of ErbB3. Serum deprivation and hypoxia in vitro caused significant down-regulation of the mRNA expression of ErbB2 and ErbB4 receptors, but the mRNA expression of ErbB3 was not changed.

Conclusion: Expression of ErbB2 and ErbB4 receptors mRNA is down-regulated in myocardial infarction, which may results from the hypoxia, deprivation of nutrients and cytokines.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Newborn
  • Cells, Cultured
  • Down-Regulation
  • ErbB Receptors / metabolism*
  • Glycoproteins / metabolism*
  • Heart Ventricles / metabolism*
  • Myocardial Infarction / metabolism*
  • Myocardial Infarction / pathology
  • Myocytes, Cardiac / cytology
  • Myocytes, Cardiac / metabolism*
  • Myocytes, Cardiac / pathology
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Receptor, ErbB-2
  • Receptor, ErbB-4

Substances

  • Glycoproteins
  • RNA, Messenger
  • ErbB Receptors
  • Erbb2 protein, rat
  • Erbb4 protein, rat
  • Receptor, ErbB-2
  • Receptor, ErbB-4