Trends in Cardiovascular Medicine
Volume 16, Issue 6 , Pages 209-215, August 2006

Versican Degradation and Vascular Disease

  • Richard D. Kenagy

      Affiliations

    • Department of Surgery, Seattle, WA 98109-4714, USA
    • Corresponding Author InformationAddress correspondence to: Richard D. Kenagy, PhD, Center for Cardiovascular Biology and Regenerative Medicine, University of Washington, Room 334, 815 Mercer St. Seattle, WA 98109, USA. Tel.: (+1) 206-897-1550; fax: (+1) 206-897-1553.
  • ,
  • Anna H. Plaas

      Affiliations

    • Department of Internal Medicine, University of South Florida, Tampa, FL 33612, USA
  • ,
  • Thomas N. Wight

      Affiliations

    • Hope Heart Program, Benaroya Research Institute at Virginia Mason, Seattle, WA 98101-2795, USA

Versican is an abundant proteoglycan in the blood vessel wall that is increased after vascular injury and accumulates in advanced atherosclerotic plaques. Versican is a large molecule with domains that mediate binding to cytokines, enzymes, lipoproteins, other extracellular matrix molecules, and signaling receptors. There is evidence that versican exists in the normal, as well as the diseased, vessel wall as discrete fragments, which represent these functional domains. We review the literature on versican degradation in vascular tissue and the function of versican domains, all of which suggest that proteolytic modification of versican may have physiologic as well as pathologic implications for the vascular system.

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PII: S1050-1738(06)00067-3

doi:10.1016/j.tcm.2006.03.011

Trends in Cardiovascular Medicine
Volume 16, Issue 6 , Pages 209-215, August 2006