title: Increased atherosclerosis in mice deficient in perilipin1.
abstract: BACKGROUND
  Perilipin1, a lipid droplet associated protein has an important role in the regulation of lipolysis and lipid storage in adipocytes. Perilipin1 is also expressed in foam cells of atheroma plaques and could therefore play a role in the accumulation of lipids in arterial wall and in the development of atherosclerosis. The aim of the study was to investigate this possible role of perilipin1 in atherogenesis.
  
  
  METHODS
  Mice deficient in perilipin1 (Plin1-/-) were crossed with Ldlr-/- mice. Ldlr-/- and Plin1-/- Ldlr-/- mice received an atherogenic diet during 10 or 20 weeks. Blood pressure and plasma lipids concentrations were measured. Aortas were collected at the end of the atherogenic diet periods for quantification of atheroma lesions (en face method), histological and immunohistological studies
  
  
  RESULTS
  Ldlr-/- and Plin1-/- Ldlr-/- mice had comparable blood pressure and plasma lipids levels. Plin1-/- Ldlr-/- mice had a lower body weight and decreased adiposity. The atherosclerotic lesion area in Plin1-/-Ldlr-/- mice was moderately increased after 10 weeks of atherogenic diet (ns) and significantly higher after 20 weeks (p < 0.01). Histology of atheroma plaques was comparable with no sign of increased inflammation in Plin1-/- Ldlr-/- mice.
  
  
  CONCLUSIONS
  Perilipin1 ablation in mice results in increased atherosclerosis independently of modifications of risk factors such as raised blood pressure or plasma lipids levels. These data strongly support an atheroprotective role for perilipin1.
authors.affiliation: ERI22-EA4173, Faculté Rockefeller, University C Bernard Lyon1, 8 av Rockefeller, Lyon, 69008, France.
authors.forename: Dominique
authors.initials: D
authors.lastname: Langlois
authors.forename: Fabien
authors.initials: F
authors.lastname: Forcheron
authors.forename: Jacques-Yuan
authors.initials: JY
authors.lastname: Li
authors.forename: Peggy
authors.initials: P
authors.lastname: del Carmine
authors.forename: Samia
authors.initials: S
authors.lastname: Neggazi
authors.forename: Michel
authors.initials: M
authors.lastname: Beylot
mesh_terms: D050154:Adiposity; D000818:Animals; D001011:Aorta / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D001025:Aortitis / Q000209:etiology; D050197:Atherosclerosis / Q000276:immunology / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D001835:Body Weight; D002352:Carrier Proteins / Q000235:genetics / Q000502:physiology*; D003433:Crosses, Genetic; D004036:Diet, Atherogenic / Q000009:adverse effects; D006949:Hyperlipidemias / Q000097:blood / Q000209:etiology; D006973:Hypertension / Q000209:etiology; D018836:Inflammation Mediators / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D000070778:Perilipin-1; D010750:Phosphoproteins / Q000235:genetics / Q000502:physiology*; D058226:Plaque, Atherosclerotic / Q000209:etiology / Q000473:pathology; D012333:RNA, Messenger / Q000378:metabolism; D011973:Receptors, LDL / Q000235:genetics / Q000502:physiology; D012720:Severity of Illness Index
chemical_list: D002352:Carrier Proteins; D018836:Inflammation Mediators; D000070778:Perilipin-1; D010750:Phosphoproteins; C000602979:Plin1 protein, mouse; D012333:RNA, Messenger; D011973:Receptors, LDL