TY - JOUR
T1 - Fucoidan is a non-anticoagulant inhibitor of intimal hyperplasia
AU - McCaffrey, Timothy A.
AU - Falcone, Domenick J.
AU - Borth, Wolfgang
AU - Brayton, Cory F.
AU - Weksler, Babette B.
N1 - Funding Information:
This work was supported in part by National Institutes of Health (NIH) grant (HL35724) to B. Weksler, NIH FIRST Award (HL42606) to T. McCaffrey, NIH Research Career Development Award (HL01962) to D. Falcone, a Specialized Center of Research in Thrombosis grant (HL18828), an NIH Program Project in Atherosclerosis (HL46403) and an NIH Training Grant (RR-07044) to C. Brayton. W. Borth is supported by the Medizinisch-Wissenschaftlicher Fonds des Burgermeisters der Bundeshauptstadt Wien.
PY - 1992/4/30
Y1 - 1992/4/30
N2 - 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.
AB - 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.
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U2 - 10.1016/0006-291X(92)90657-7
DO - 10.1016/0006-291X(92)90657-7
M3 - Article
C2 - 1315533
AN - SCOPUS:0026694618
SN - 0006-291X
VL - 184
SP - 773
EP - 781
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 2
ER -