title: Serum starvation and growth factor receptor expression in vascular smooth muscle cells.
abstract: BACKGROUND
  Smooth muscle cell (SMC) proliferation in atherosclerosis is regulated through the interaction of growth factors like platelet-derived growth factor-BB (PDGF-BB) and insulin-like growth factor-1 (IGF-1) and their receptors (R). We hypothesized that serum starvation of SMCs may affect PDGFbeta-R and IGF-1-R expression and, consequently, the effect of their cognate ligands on SMC survival/proliferation.
  
  
  RESULTS
  Serum starvation significantly increases PDGFbeta-R but not IGF-1-R mRNA and protein expression in SMCs. PDGF-BB stimulates cell survival but not proliferation in serum-starved SMCs of the synthetic phenotype, whereas SMCs of the contractile phenotype respond to PDGF-BB by a significant increase in proliferation. Immunohistochemical analysis of coronary atherosclerotic lesions reveals PDGFbeta-R expression in SMCs in the lamina fibromuscularis, but not in the media and in healthy parts of the arterial wall. No such differential expression was observed for IGF-1-R.
  
  
  CONCLUSIONS
  Differential regulation of PDGFbeta-R and IGF-1-R expression by serum starvation might represent a mechanism for the control of SMC survival/proliferation in atherogenesis and restenosis. The distribution of PDGFbeta-Rs and IGF-1-Rs in atherosclerotic lesions may indicate an effect of serum starvation on SMCs in the arterial wall.
authors.affiliation: Center for Cell and Gene Therapy, and Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Tex., USA. oliver.zimmermann@medizin.uni-ulm.de
authors.forename: Oliver
authors.initials: O
authors.lastname: Zimmermann
authors.forename: Thomas P
authors.initials: TP
authors.lastname: Zwaka
authors.forename: Nikolaus
authors.initials: N
authors.lastname: Marx
authors.forename: Michael
authors.initials: M
authors.lastname: Torzewski
authors.forename: Andrea
authors.initials: A
authors.lastname: Bucher
authors.forename: Peter
authors.initials: P
authors.lastname: Guilliard
authors.forename: Andreas
authors.initials: A
authors.lastname: Hannekum
authors.forename: Vinzenz
authors.initials: V
authors.lastname: Hombach
authors.forename: Jan
authors.initials: J
authors.lastname: Torzewski
mesh_terms: D000077214:Becaplermin; D049109:Cell Proliferation; D002478:Cells, Cultured; D003324:Coronary Artery Disease / Q000473:pathology / Q000503:physiopathology; D016895:Culture Media, Serum-Free; D015536:Down-Regulation; D006801:Humans; D009131:Muscle, Smooth, Vascular / Q000166:cytology* / Q000503:physiopathology*; D010982:Platelet-Derived Growth Factor / Q000494:pharmacology; D020574:Proto-Oncogene Proteins c-sis; D017526:Receptor, IGF Type 1 / Q000096:biosynthesis*; D020797:Receptor, Platelet-Derived Growth Factor beta / Q000096:biosynthesis*; D015854:Up-Regulation
chemical_list: D016895:Culture Media, Serum-Free; D010982:Platelet-Derived Growth Factor; D020574:Proto-Oncogene Proteins c-sis; D000077214:Becaplermin; D017526:Receptor, IGF Type 1; D020797:Receptor, Platelet-Derived Growth Factor beta