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Fem1a is a mitochondrial protein up‐regulated upon ischemia–reperfusion injury
Author(s) -
Cambier Linda,
Lacampagne Alain,
Auffray Charles,
Pomiès Pascal
Publication year - 2009
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2009.04.035
Subject(s) - myocyte , immunofluorescence , mitochondrion , microbiology and biotechnology , c2c12 , reperfusion injury , ischemia , cardiac muscle , receptor , subcellular localization , biology , chemistry , antibody , medicine , endocrinology , biochemistry , cytoplasm , immunology , myogenesis
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.