Arterial smooth muscle cells in vivo: relationship between actin isoform expression and mitogenesis and their modulation by heparin.

• DOI: 10.1083/jcb.107.5.1939
• Publication Date: 2004-05-15T00:18:20Z
• Authors: A W Clowes; M M Clowes; O Kocher; P Ropraz; C Chaponnier; G Gabbiani
• Keywords: Male; Muscle, Smooth, Vascular/ cytology/drug effects/enzymology; 0303 health sciences; Cell Division/drug effects; Heparin; info:eu-repo/classification/ddc/616.07; Actins/ biosynthesis/genetics; Cell Cycle; Rats, Inbred Strains; Cell Separation; ddc:616.07; Blotting, Northern; Actins; Muscle, Smooth, Vascular; Rats; 3. Good health; 03 medical and health sciences; RNA/isolation & purification; Heparin/ pharmacology; Animals; RNA; Electrophoresis, Polyacrylamide Gel; Cell Division

Quiescent smooth muscle cells (SMC) in normal artery express a pattern of actin isoforms with alpha-smooth (alpha SM) predominance that switches to beta when the are proliferating. We have examined relationship between change and entry SMC into growth cycle an vivo model proliferation (balloon injured rat carotid artery). alpha SM mRNA declined cytoplasmic (beta + gamma) mRNAs increased early G0/G1 (between 1 8 h after injury). In synthesis vitro translation experiments demonstrated functional is decreased 24 injury proportional amount present. At 36 injury, prepared by enzymatic digestion were sorted S/G2 populations; only committed proliferate (S/G2 fraction) showed relative slight decrease and, more importantly, large mRNA. A switch from was present whole population 5 d injury. To determine if associated proliferation, we inhibited approximately 80% heparin, which has previously been shown block late reduce fraction. The at not prevented; however, protein reinduced heparin-treated animals compared saline-treated controls. These results suggest arterial depends on levels changes whether or subsequently proliferate. prevented but they eventually reversed kept resting state heparin treatment.