title: Leptin promotes vascular remodeling and neointimal growth in mice.
abstract: OBJECTIVE
  Human obesity is associated with elevated leptin levels and a high risk of death from cardiovascular disease. In the present study, we investigated the effects of leptin on vascular wound healing and arterial lesion growth in mice.
  
  
  RESULTS
  Wild-type mice placed on an atherogenic, high-fat diet had elevated (9-fold) leptin levels compared with their counterparts maintained on normal chow, and the former demonstrated significantly enhanced neointimal thickening after carotid artery injury with ferric chloride. The lesions forming in response to injury strongly expressed leptin receptor mRNA and protein. Unexpectedly, the atherogenic diet had no effect on injured vessels from leptin-deficient ob/ob mice despite aggravating obesity, diabetes, and hyperlipidemia in these animals. Daily administration of leptin to ob/ob mice during the 3-week period after injury reversed this phenotype, dramatically increasing neointimal thickness and the severity of luminal stenosis. Exogenous leptin also enhanced lesion growth and increased cellular proliferation in injured arteries from wild-type mice but had no effect on vessels from leptin receptor-deficient db/db mice.
  
  
  CONCLUSIONS
  Our results raise the possibility that there might be a direct, leptin receptor-mediated link between the hyperleptinemia in human obesity and the increased risk for cardiovascular complications associated with this condition.
authors: Department of Cardiology and Pulmonary Medicine, University of Goettingen, Goettingen, Germany.
authors: Katrin
authors: K
authors: Schäfer
authors: Martin
authors: M
authors: Halle
authors: Colin
authors: C
authors: Goeschen
authors: Claudia
authors: C
authors: Dellas
authors: Marianne
authors: M
authors: Pynn
authors: David J
authors: DJ
authors: Loskutoff
authors: Stavros
authors: S
authors: Konstantinides
mesh_terms: D000818:Animals; D001011:Aorta / Q000166:cytology; D001161:Arteriosclerosis / Q000378:metabolism; D002339:Carotid Arteries / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D002712:Chlorides; D004036:Diet, Atherogenic; D004041:Dietary Fats / Q000009:adverse effects; D004195:Disease Models, Animal; D005290:Ferric Compounds / Q000633:toxicity; D005786:Gene Expression Regulation; D006965:Hyperplasia; D020738:Leptin / Q000172:deficiency / Q000235:genetics / Q000494:pharmacology / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D009131:Muscle, Smooth, Vascular / Q000378:metabolism* / Q000473:pathology; D009765:Obesity / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis; D011956:Receptors, Cell Surface / Q000096:biosynthesis / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D054411:Receptors, Leptin; D011994:Recombinant Proteins / Q000494:pharmacology; D017539:Tunica Intima / Q000473:pathology*
chemical_list: D002712:Chlorides; D004041:Dietary Fats; D005290:Ferric Compounds; C515448:LEPR protein, human; D020738:Leptin; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin; D011994:Recombinant Proteins; C515447:leptin receptor, mouse; C024555:ferric chloride