Collagen suppresses the proliferative phenotype of allylamine-injured vascular smooth muscle cells

Emily Wilson, Alan R. Parrish, Christopher M. Bral, E. Spencer Williams, Kenneth Ramos

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Repeated cycles of oxidative injury by allylamine induce proliferative rat vascular smooth muscle cell (vSMC) phenotypes characterized by enhanced secretion of osteopontin (OPN). The present study was designed to evaluate the role of extracellular matrix (ECM) interactions in the induction of proliferative phenotypes in this model of oxidant injury. Because OPN is involved in ECM/integrin signaling, and may participate in proliferative control, the proliferation profiles of control and allylamine vSMCs seeded on different matrices were compared. Allylamine cells exhibited a proliferative advantage over controls when seeded on plastic, Pronectin, or fibronectin, but not type I collagen. Addition of GRGDS peptide selectively enhanced [3H]-thymidine incorporation in allylamine vSMCs, while anti-OPN antibodies nullified their proliferative advantage. Allylamine cells exhibited altered expression of α1, α5 and β3 integrin subunits and enhanced downstream integrin-coupled increases in focal adhesion kinase, AP-1 and NF-κB binding activity. Inhibition of NF-κB by pyrrolidine dithiocarbamate selectively compromised proliferation of allylamine vSMCs, while seeding on a non-permissive collagen matrix ablated enhancement of NF-κB inducibility. These results implicate ECM interactions in the deregulation of vSMC proliferation following repeated cycles of oxidative chemical injury.

Original languageEnglish (US)
Pages (from-to)289-297
Number of pages9
JournalAtherosclerosis
Volume162
Issue number2
DOIs
StatePublished - 2002
Externally publishedYes

Fingerprint

Allylamine
Vascular Smooth Muscle
Smooth Muscle Myocytes
Collagen
Phenotype
Osteopontin
Integrins
Extracellular Matrix
Focal Adhesion Kinase 1
glycyl-arginyl-glycyl-aspartyl-serine
Wounds and Injuries
Transcription Factor AP-1
Collagen Type I
Fibronectins
Oxidants
Thymidine
Plastics
Anti-Idiotypic Antibodies
Cell Proliferation
Peptides

Keywords

  • NF-κB
  • Osteopontin
  • Vascular smooth muscle cell

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Collagen suppresses the proliferative phenotype of allylamine-injured vascular smooth muscle cells. / Wilson, Emily; Parrish, Alan R.; Bral, Christopher M.; Williams, E. Spencer; Ramos, Kenneth.

In: Atherosclerosis, Vol. 162, No. 2, 2002, p. 289-297.

Research output: Contribution to journalArticle

Wilson, Emily ; Parrish, Alan R. ; Bral, Christopher M. ; Williams, E. Spencer ; Ramos, Kenneth. / Collagen suppresses the proliferative phenotype of allylamine-injured vascular smooth muscle cells. In: Atherosclerosis. 2002 ; Vol. 162, No. 2. pp. 289-297.
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