title: A variant derived from rabbit aortic smooth muscle: phenotype modulation and restoration of smooth muscle characteristics in cells in culture.
abstract: We examined the relationship between growth arrest of smooth muscle cells and structural changes in microfilament bundles, and also that between the structural changes and the actions of contractile agonist using a multipassagable variant cell line (SM-3) derived from rabbit aortic smooth muscle cells. The content of smooth muscle type alpha-actin increased with density-dependent growth arrest of the SM-3 cells, but was attenuated in the logarithmically growing cultures. As assessed cytochemically, the growth-arrested cells contained longitudinally oriented bundles of actin-containing microfilament and myosin-based filaments visualized with rhodamine-phalloidin and antibody against myosin light chain 20, respectively, whereas both actin- and myosin-containing structures in logarithmically growing cells showed slight, shortened, or diffused patterns. Electron microscopic examination of the growth-arrested cells revealed that the cells contained numerous and conspicuous microfilament bundles associated with many compact electron-dense bodies. In addition, pinocytotic vesicles were often found near the plasma membrane in the growth-arrested cells. SM-3 cells in the growth-arrested phase responded to prostaglandin F2 alpha (3-30 microM) and rat endothelin (0.1-1.0 microM) with a reversible contractile response, in association with monophosphorylation and/or diphosphorylation of the myosin light chain 20. However, the influence of the contractile agonists was greatly reduced during logarithmic growth. These results suggest that in the SM-3 cells in the growth-arrested phase, there is a restoration of the contractile architecture and the myosin light chain phosphorylation system. Thus, this SM-3 cell line is expected to serve as a useful model for examining biochemical and physiological phenomena of smooth muscle.
authors.affiliation: Life Science Center, Biochemical Research Lab., Asahi Chemical Industry, Miyazaki.
authors.forename: Y
authors.initials: Y
authors.lastname: Sasaki
authors.forename: T
authors.initials: T
authors.lastname: Uchida
authors.forename: Y
authors.initials: Y
authors.lastname: Sasaki
mesh_terms: D000199:Actins / Q000096:biosynthesis; D000818:Animals; D001011:Aorta / Q000166:cytology; D002455:Cell Division; D002478:Cells, Cultured; D003470:Culture Media; D003599:Cytoskeleton / Q000378:metabolism; D015237:Dinoprost / Q000494:pharmacology; D014644:Genetic Variation; D006651:Histocytochemistry; D009119:Muscle Contraction / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000166:cytology*; D010641:Phenotype; D011817:Rabbits
chemical_list: D000199:Actins; D003470:Culture Media; D015237:Dinoprost