title: APEG-1, a novel gene preferentially expressed in aortic smooth muscle cells, is down-regulated by vascular injury.
abstract: 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. The cDNA of rat APEG-1 contained an open reading frame encoding 113 amino acids, which would predict a basic protein of 12.7 kDa. The amino acid sequence of rat APEG-1 was highly conserved among 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. By in situ hybridization, APEG-1 mRNA was expressed in rat ASMC. Although APEG-1 was expressed highly in differentiated ASMC in vivo, its expression was quickly down-regulated and disappeared in dedifferentiated ASMC in culture. In vivo, APEG-1 mRNA levels decreased by more than 80% 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.
authors.affiliation: Department of Medicine, Harvard Medical School, Pulmonary and Cardiovascular Divisions, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.
authors.forename: C M
authors.initials: CM
authors.lastname: Hsieh
authors.forename: M
authors.initials: M
authors.lastname: Yoshizumi
authors.forename: W O
authors.initials: WO
authors.lastname: Endege
authors.forename: C J
authors.initials: CJ
authors.lastname: Kho
authors.forename: M K
authors.initials: MK
authors.lastname: Jain
authors.forename: S
authors.initials: S
authors.lastname: Kashiki
authors.forename: R
authors.initials: R
authors.lastname: de los Santos
authors.forename: W S
authors.initials: WS
authors.lastname: Lee
authors.forename: M A
authors.initials: MA
authors.lastname: Perrella
authors.forename: M E
authors.initials: ME
authors.lastname: Lee
mesh_terms: D000595:Amino Acid Sequence; D000818:Animals; D001011:Aorta / Q000293:injuries / Q000378:metabolism; D001483:Base Sequence; D005075:Biological Evolution; D002478:Cells, Cultured; D003001:Cloning, Molecular; D016384:Consensus Sequence; D017124:Conserved Sequence; D017931:DNA Primers; D005786:Gene Expression Regulation; D006801:Humans; D017403:In Situ Hybridization; D008297:Male; D051379:Mice; D008969:Molecular Sequence Data; D008970:Molecular Weight; D009124:Muscle Proteins / Q000096:biosynthesis* / Q000737:chemistry; D009131:Muscle, Smooth, Vascular / Q000293:injuries* / Q000378:metabolism*; D009219:Myosin-Light-Chain Kinase; D016366:Open Reading Frames; D009928:Organ Specificity; D016133:Polymerase Chain Reaction; D017346:Protein Serine-Threonine Kinases; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D011994:Recombinant Proteins / Q000096:biosynthesis / Q000737:chemistry; D017386:Sequence Homology, Amino Acid; D016324:Sequence Tagged Sites; D014158:Transcription, Genetic
chemical_list: D017931:DNA Primers; D009124:Muscle Proteins; D012333:RNA, Messenger; D011994:Recombinant Proteins; D017346:Protein Serine-Threonine Kinases; C100675:SPEG protein, human; C484400:Speg protein, mouse; C484401:Speg protein, rat; D009219:Myosin-Light-Chain Kinase