(Circulation. 2001;103:2501.)
© 2001 American Heart Association, Inc.
Basic Science Reports |
ß3-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
From the Department of Medicine (S.S.S., B.S.C.), Department of Surgery (E.D.R., W.Z.), and Department of Pathology (J.T.F., R.E.G.), Mount Sinai School of Medicine, New York, NY.
Correspondence to Barry S. Coller, MD, Department of Medicine, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029. E-mail Barry.Coller{at}mssm.edu
Background—Intimal
hyperplasia contributes to restenosis after
percutaneous vascular interventions. Both
ß3-integrins,
Vß3 and
IIbß3
(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, ß3-integrin–deficient mice, and P-selectin–deficient mice were studied in a model of transluminal endothelial injury of the femoral artery. At 4 weeks, ß3-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 ß3-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 ß3-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.
Key Words: cell adhesion molecules • leukocytes • platelets • receptors • restenosis
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