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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:2027.)
© 2003 American Heart Association, Inc.

Vascular Biology

Neointimal Formation After Endovascular Arterial Injury Is Markedly Attenuated in db/db Mice

Kent Stephenson; James Tunstead; Aileen Tsai; Ronald Gordon; Scott Henderson; Hayes M. Dansky

From the Departments of Medicine (K.S., J.T., A.T., H.M.D.) and Pathology (R.G.), Microscopy Shared Resource Facility (S.H.), Brookdale Department of Molecular, Cell and Developmental Biology (S.H.), and the Zena and Michael A. Wiener Cardiovascular Institute (K.S., J.T., A.T., H.M.D.), New York, NY.

Correspondence to Hayes M. Dansky, MD, Cardiovascular Institute, Box 1269, Mount Sinai School of Medicine, One Gustave Levy Place, New York, NY 10029. E-mail hayes.dansky{at}mssm.edu

Objective— A diabetic mouse model of accelerated neointimal formation would be a useful tool to understand the increased incidence of restenosis in patients with diabetes.

Methods and Results— Femoral artery endoluminal wire injury was performed in diabetic insulin 2 Akita (ins2^Akita) and leptin receptor db/db (lepr^db/db) mutant mice. Neointima size in ins2^Akita mouse arteries was unchanged compared with nondiabetic wild-type littermates. Although Ki67 labeling demonstrated similar rates of replication in the neointima of lepr^db/db mouse arteries, neointimal formation in lepr^db/db mice was surprisingly reduced by 90% compared with nondiabetic lepr^+/+ mice. Four hours after arterial injury, medial smooth muscle cell death was diminished in lepr^db/db arteries, suggesting that the initial response to arterial injury was altered in lepr^db/db mice.

Conclusions— These studies highlight a differential response to arterial injury in lepr^db/db mice and suggest a potential role for leptin in the regulation of neointimal formation in response to arterial injury.

Key Words: leptin • diabetes • arterial injury • smooth muscle cell proliferation • restenosis

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