on September 18, 2003
Published online before print September 18, 2003, doi: 10.1161/01.ATV.0000096394.32433.E9
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Submitted on September 3, 2003
Accepted on September 9, 2003
Neointimal Formation After Endovascular Arterial Injury Is Markedly Attenuated in db/db Mice
Kent Stephenson ;
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.
* To whom correspondence should be addressed. 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 (ins2Akita) and leptin receptor db/db (leprdb/db) mutant mice. Neointima size in ins2Akita mouse arteries was unchanged compared with nondiabetic wild-type littermates. Although Ki67 labeling demonstrated similar rates of replication in the neointima of leprdb/db mouse arteries, neointimal formation in leprdb/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 leprdb/db arteries, suggesting that the initial response to arterial injury was altered in leprdb/db mice.
Conclusions--These studies highlight a differential response to arterial injury in leprdb/db mice and suggest a potential role for leptin in the regulation of neointimal formation in response to arterial injury.
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