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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20:1488.)
© 2000 American Heart Association, Inc.

Vascular Biology

₂-Antiplasmin Gene Deficiency in Mice Does Not Affect Neointima Formation After Vascular Injury

H. R. Lijnen; B. Van Hoef; M. Dewerchin; D. Collen

From the Center for Molecular and Vascular Biology (H.R.L., B.V.H., D.C.), University of Leuven, and the Center for Transgene Technology and Gene Therapy (M.D., D.C.), Flanders Interuniversity Institute for Biotechnology, Leuven, Belgium.

Correspondence to H. R. Lijnen, PhD, Center for Molecular and Vascular Biology, University of Leuven, Campus Gasthuisberg, O & N, Herestraat 49, B-3000 Leuven, Belgium. E-mail roger.lijnen{at}med.kuleuven.ac.be

Abstract—The hypothesis that ₂-antiplasmin (₂-AP), the main physiological plasmin inhibitor, plays a role in neointima formation was tested with use of a vascular injury model in wild-type (₂-AP^+/+) and ₂-AP–deficient (₂-AP^-/-) mice. The neointimal and medial areas were similar 1 to 3 weeks after electric injury of the femoral artery in ₂-AP^+/+ and ₂-AP^-/- mice, resulting in comparable intima/media ratios (eg, 0.43±0.12 and 0.42±0.11 2 weeks after injury). Nuclear cell counts in cross-sectional areas of the intima of the injured region were also comparable in arteries from ₂-AP^+/+ and ₂-AP^-/- mice (78±19 and 69±8). Fibrin deposition was not significantly different in arteries of both genotypes 1 day after injury, and no mural thrombosis was detected 1 week after injury. Fibrinolytic activity in femoral arterial sections, as monitored by fibrin zymography, was higher in ₂-AP^-/- mice 1 week after injury (P<0.001) but was comparable in both genotypes 2 and 3 weeks after injury. Staining for elastin did not reveal significant degradation of the internal elastica lamina in either genotype. Immunocytochemical analysis revealed a comparable distribution pattern of -actin–positive smooth muscle cells in both genotypes. These findings indicate that the endogenous fibrinolytic system of ₂-AP^+/+ mice is capable of preventing fibrin deposition after vascular injury and suggest that ₂-AP does not play a major role in smooth muscle cell migration and neointima formation in vivo.

Key Words: neointima • restenosis • transgenic mice • ₂-antiplasmin

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