Despite the importance of phenotypic alterations in arterial smooth muscle cells (ASMC) during the pathogenesis of arteriosclerosis, little is known about genes that define differentiated ASMC. Using differential mRNA display, we isolated a novel gene preferentially expressed in the rat aorta and termed this gene APEG-1. By in situ hybridization, APEG-1 mRNA was expressed in ASMC but not in visceral smooth muscle cells of the colon. The cDNA of rat APEG-1 contained an open reading frame encoding 113 amino acids that would predict a basic protein of 12.7 kDa. The protein sequence of rat APEG-1 was highly conserved among the human and mouse homologues (97% and 98% respectively). Using an APEG-1 fusion protein containing an N-terminal c-myc tag, we identified APEG-1 as a nuclear protein. Although APEG-1 was expressed highly in differentiated ASMC in vivo, its expression was quickly downregulated and disappeared in dedifferemiated ASMC in culture. In vivo, APEG-1 mRNA levels decreased by more than 75% in response to vascular injury as ASMC changed from a quiescent to a proliferative phenotype. Taken together, these data indicate that APEG-1 is a novel marker for differentiated ASMC and may have a role in regulating growth and differentiation of this cell type. Supported by grants from the National Institutes of Health and Bristol-Myers Squibb.
|Publication status||Published - 1996|
ASJC Scopus subject areas
- Agricultural and Biological Sciences (miscellaneous)
- Biochemistry, Genetics and Molecular Biology(all)
- Cell Biology