Fem1a is a mitochondrial protein up-regulated upon ischemia-reperfusion injury

FEBS Lett. 2009 May 19;583(10):1625-30. doi: 10.1016/j.febslet.2009.04.035. Epub 2009 May 4.

Abstract

Various expression studies have shown a preferential muscle expression of the mouse Fem1a gene, but no data is available on the subcellular localization of the corresponding protein. Here, using a specific antibody, we show that Fem1a is expressed preferentially in cardiac muscle, brain and liver. Moreover, using immunofluorescence and electron microscopy, as well as biochemical assays, we demonstrate that Fem1a is localized within mitochondria of C2C12 myoblasts and cardiac muscle cells. Finally, we show that the expression of Fem1a, which is a cellular partner of the EP4 receptor for prostaglandin E(2), is increased in mouse hearts after myocardial infarction.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Cycle Proteins / genetics*
  • Cell Cycle Proteins / metabolism
  • HeLa Cells
  • Humans
  • Mice
  • Mitochondrial Proteins / genetics*
  • Mitochondrial Proteins / metabolism
  • Myocardial Reperfusion Injury / genetics*
  • Myocardial Reperfusion Injury / metabolism
  • Up-Regulation*

Substances

  • Cell Cycle Proteins
  • FEM1A protein, human
  • Mitochondrial Proteins