The EAT/mcl-1 gene, an inhibitor of apoptosis, is up-regulated in the early stage of acute myocardial infarction

Biochim Biophys Acta. 1999 Nov 16;1472(3):471-8. doi: 10.1016/s0304-4165(99)00149-x.

Abstract

EAT/mcl-1 (EAT), a bcl-2-related immediate early gene, is up-regulated at an early stage of differentiation of human embryonal carcinoma cells. Recent studies have revealed that EAT inhibits apoptosis both in vitro and in vivo. In the present study, we demonstrated that the EAT gene was up-regulated in the early stage of rat myocardial infarction. This pattern of up-regulation was apparently different from that of another immediate early gene, c-fos. EAT, an anti-apoptotic molecule, was strongly up-regulated in the non-ischemic region. In contrast, the expression of c-fos was induced in both ischemic and non-ischemic regions, and was higher in the ischemic region. Apoptosis of cardiomyocytes is currently thought to significantly contribute to acute myocardial infarction. We detected cardiomyocyte apoptosis by gel electrophoresis of genomic DNA and in situ nick end labeling in the ischemic region, but not in the non-ischemic region. As an inhibitor of apoptosis, EAT may play a role in the protection of cardiomyocytes in the early stage of acute myocardial infarction.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / genetics*
  • Disease Models, Animal
  • In Situ Nick-End Labeling
  • Male
  • Myeloid Cell Leukemia Sequence 1 Protein
  • Myocardial Infarction / genetics*
  • Myocardial Infarction / metabolism
  • Myocardium / metabolism
  • Neoplasm Proteins / biosynthesis
  • Neoplasm Proteins / genetics*
  • Proto-Oncogene Proteins c-bcl-2*
  • RNA, Messenger / biosynthesis
  • Rats
  • Rats, Wistar
  • Up-Regulation

Substances

  • Myeloid Cell Leukemia Sequence 1 Protein
  • Neoplasm Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • RNA, Messenger