β3-integrin-deficient mice but not P-selectin-deficient mice develop intimal hyperplasia after vascular injury: Correlation with leukocyte recruitment to adherent platelets 1 hour after injury

Susan S. Smyth, Ernane D. Reis, Wen Zhang, John T. Fallon, Ronald E. Gordon, Barry S. Coller

Research output: Contribution to journalArticlepeer-review

134 Scopus citations

Abstract

Background - Intimal hyperplasia contributes to restenosis after percutaneous vascular interventions. Both β3-integrins, αvβ3 and αIIbβ3 (glycoprotein IIb/IIIa), and leukocytes have been implicated in neointimal formation, based in part on the results obtained using antagonists to 1 or both receptors in animal models. Methods and Results - The responses in wild-type mice, β3-integrin-deficient mice, and P-selectin-deficient mice were studied in a model of transluminal endothelial injury of the femoral artery. At 4 weeks, β3-integrin-deficient mice were not protected from developing intimal hyperplasia, whereas P-selectin-deficient mice were protected, Within 1 hour of injury, several layers of platelets deposited on the arteries of wild-type mice and a single layer of platelets deposited on the vessels of β3-integrin-deficient mice; in both cases, leukocytes were recruited to the platelet layer. In P-selectin-deficient mice, the platelet layer was less compact and extended further into the lumen but did not recruit leukocytes. Conclusions - In a model of transluminal arterial injury, absence of early leukocyte recruitment and not deficiency of β3-integrins correlated with a reduction in neointimal formation. Blockade of P-selectins may be an effective therapeutic strategy to decrease restenosis after percutaneous vascular interventions.

Original languageEnglish
Pages (from-to)2501-2507
Number of pages7
JournalCirculation
Volume103
Issue number20
DOIs
StatePublished - 22 May 2001

Keywords

  • Cell adhesion molecules
  • Leukocytes
  • Platelets
  • Receptors
  • Restenosis

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