on March 8, 2004
Published online before print March 8, 2004, doi: 10.1161/01.CIR.0000121733.68724.FF
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Submitted on September 3, 2002
From the Departments of Surgery (E.T.C., J.E.L., E.T.C., K.P.B., B.R.V.), Internal Medicine (M.F.K., D.R.A.), Pediatrics (W.C.P.), Cell Biology and Physiology (W.C.P., D.R.A.), and Pathology (D.V.N.), Washington University School of Medicine, St Louis, Mo. * To whom correspondence should be addressed. E-mail: choie{at}msnotes.wustl.edu.
Background--Pharmacological blockade of Methods and Results--After disruption of the carotid with a transluminal probe, there was no significant difference in neointimal thickening between Conclusions--The
Revised on December 1, 2003
Accepted on December 4, 2003
Eric T. Choi MD*, 
3-Integrin Mediates Smooth Muscle Cell Accumulation in Neointima After Carotid Ligation in Mice
3-integrins inhibits neointimal lesion formation in nonmouse animal models of arterial injury. In contrast, 3-integrin-deficient (3-/-) mice are not protected from neointimal lesion formation after arterial injury. We investigated this discrepancy in 3-/- and wild-type (3+/+) mice using different models of injury.3-/- and 3+/+ mice. However, after ligation of the carotid without medial disruption, there was reduced neointimal thickening in 3-/- mice compared with 3+/+ mice at intervals up to 3 months. Lesion reduction in 3-/- mice was associated with fewer intimal smooth muscle cells (SMCs) without a difference in SMC apoptosis or proliferation rate compared with 3+/+ mice, consistent with reduced SMC migration from the media into the intima of 3-/- mice. Moreover, combined eccentric medial disruption and ligation of the carotid in 3-/- mice resulted in neointimal lesion formation only at the site of medial disruption. Transplantation of bone marrow cells harvested from 3+/+ mice into irradiated 3-/- mice resulted in reduced neointimal lesion formation after carotid ligation injury, confirming the importance of 
v3 and not IIb3 in the attenuated response.v3-integrin mediates intimal SMC accumulation that contributes to neointimal thickening in the setting of arterial ligation.
Key words: restenosis • cell adhesion molecules • muscle, smooth • angioplasty
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