Fucoidan is a non-anticoagulant inhibitor of intimal hyperplasia

Timothy A. McCaffrey, Domenick J. Falcone, Wolfgang Borth, Cory F. Brayton, Babette B. Weksler

Research output: Contribution to journalArticlepeer-review

Abstract

We previously reported that heparin inhibits the proliferation of fibroblasts and vascular smooth muscle cells (SMC), in part, by binding to and increasing the antiproliferative activity of transforming growth factor-β1 (TGF-β1). We now report that certain other polyanions which are structurally distinct from heparin, such as fucoidan and polyinosinic acid, are more avid ligands for TGF-β1 and more potent antiproliferative agents than heparin. Fucoidan possessed more potent antiproliferative activity than heparin against rat and bovine aortic SMC in vitro, though possessing much lower anticoagulant activity than heparin. Furthermore, fucoidan suppressed in vivo intimal hyperplasia when continuously infused into rats subjected to balloon-catheter injury. Unlike heparin, which also suppressed intimal hyperplasia, fucoidan did not cause systemic anticoagulation. Thus, fucoidan may be useful as a non-anticoagulant inhibitor of post-angioplasty intimal hyperplasia.

Original languageEnglish (US)
Pages (from-to)773-781
Number of pages9
JournalBiochemical and Biophysical Research Communications
Volume184
Issue number2
DOIs
StatePublished - Apr 30 1992
Externally publishedYes

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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