Increased plasmin and serine proteinase activity during flow-induced intimal atrophy in baboon PTFE grafts

Richard D. Kenagy, Jens W. Fischer, Mark G. Davies, Scott A. Berceli, Suzanne M. Hawkins, Thomas N. Wight, Alexander W. Clowes

Research output: Contribution to journalArticlepeer-review

54 Scopus citations


High blood flow causes intimal atrophy and loss of extracellular matrix in PTFE aortoiliac grafts. We have investigated whether matrix-degrading proteinases are altered in this baboon model of atrophy using zymography, western analysis, and a versican degradation assay. After four days of high flow, urokinase was increased and plasminogen activator inhibitor-1 was decreased in the intima. Plasminogen was increased after seven days. Pro-matrix metalloproteinase (MMP)-2, activated MMP-2, and proMMP-9 levels were modestly increased by high flow at 7 days, whereas MMP-3 and tissue inhibitor of metalloproteinases-1 were not altered. Extracts of 4-day high-flow intimas degraded more 35S-methionine-labeled versican than low-flow intimal extracts, and this activity was inhibited by AEBSF, a serine proteinase inhibitor, and a plasmin antibody. In contrast, this activity was not inhibited by the MMP inhibitor, BB-94 (Batimastat). These data suggest that serine proteinases, including plasmin, may be largely responsible for extracellular matrix degradation in this primate model of flow-induced intimal atrophy.

Original languageEnglish (US)
Pages (from-to)400-404
Number of pages5
JournalArteriosclerosis, Thrombosis, and Vascular Biology
Issue number3
StatePublished - 2002


  • Flow
  • Intimal atrophy
  • Plasminogen
  • Proteoglycan
  • Smooth muscle cells
  • Urokinase

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine


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