Smooth Muscle Cell Immediate‐Early Gene and Growth Factor Activation Follows Vascular InjuryA Putative In Vivo Mechanism for Autocrine Growth
作者:
Joseph Miano,
Niksa Vlasic,
Robert Tota,
Michael Stemerman,
期刊:
Arteriosclerosis and Thrombosis: A Journal of Vascular Biology
(OVID Available online 1993)
卷期:
Volume 13,
issue 2
页码: 211-219
ISSN:1049-8834
年代: 1993
出版商: OVID
关键词: immediate-early gene;growth factors;smooth muscle cell proliferation;vascular injury;autocrine growth
数据来源: OVID
摘要:
To understand the molecular events governing smooth muscle cell (SMC) proliferation in vivo, immediate-early gene (IEG) expression was assessed and related to growth factor ligand and receptor mRNA and SMC DNA synthesis after aortic injury. Balloon catheter injury evoked increases in SMCc-mycand thrombospondin(tsp)within 2 hours. The induction of these IEGs was followed by elevated transcripts to platelet-derived growth factor-A (PDGF-A), transforming growth factor-/31 (TGF-01) and a basic fibroblast growth factor (bFGF) receptor. Whereas PDGF type-/? receptor mRNA was demonstrated in SMCs from control and balloon-injured aortas, no detectable signal was observed for the PDGF type-a receptor. To explore the potential linkage between LEG products and growth factor mRNA expression, cycloheximide was employed to block early protein synthesis after balloon injury. Induction of PDGF-A and TGF-01 was attenuated by cycloheximide, but bFGF induction was unaffected. Moreover, cycloheximide superinduced IEGs and revealed PDGF-B transcripts, which were otherwise undetected. Seven days after aortic injury, a spontaneous increase inc-mycandtspmRNA was noted. This IEG reactivation was followed 12 hours later by a twofold increase in SMC DNA synthesis. These findings corroborate an autocrine mode of SMC proliferation in vivo and suggest that IEG products may control such growth by stimulating growth factor genes.
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