Neointimal formation after endovascular arterial injury is markedly attenuated in db/db mice.
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.


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 approximately 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.
D000818:Animals; D023903:Coronary Restenosis / Q000503:physiopathology; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology*; D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology*; D004195:Disease Models, Animal; D005260:Female; D005263:Femoral Artery / Q000293:injuries / Q000473:pathology / Q000503:physiopathology; D020738:Leptin / Q000502:physiology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D009131:Muscle, Smooth, Vascular / Q000293:injuries* / Q000473:pathology / Q000503:physiopathology; D009389:Neovascularization, Pathologic / Q000503:physiopathology*; D012737:Sex Factors; D017539:Tunica Intima / Q000473:pathology* / Q000503:physiopathology*; D017540:Tunica Media / Q000473:pathology
D020738:Leptin