title: Lack of interleukin-1beta decreases the severity of atherosclerosis in ApoE-deficient mice.
abstract: OBJECTIVE
  Atherosclerosis is considered to be a chronic inflammatory disease and many cytokines participate in the development of atherosclerosis. We focused on the role of interleukin-1beta (IL-1beta), one of the proinflammatory cytokines secreted by monocytes/macrophages, in the progression of atherosclerosis.
  
  
  RESULTS
  We generated mice lacking both apoE and IL-1beta. The sizes of atherosclerotic lesions at the aortic sinus in apoE-/-/IL-1beta-/-mice at 12 and 24 weeks of age showed a significant decrease of approximately 30% compared with apoE-/-/IL-1beta+/+ mice, and the percentage of the atherosclerotic area to total area of apoE-/-/IL-1beta-/- at 24 weeks of age also showed a significant decrease of about 30% compared with apoE-/-/IL-1beta+/+. The mRNA levels of vascular cell adhesion molecule (VCAM)-1 and monocyte chemotactic protein-1 in the apoE-/-/IL-1beta-/- aorta were significantly reduced compared with the apoE-/-/IL-1beta+/+. Furthermore, VCAM-1 was also reduced at the protein level in apoE-/-/IL-1beta-/- aorta compared with apoE-/-/IL-1beta+/+.
  
  
  CONCLUSIONS
  The lack of IL-1beta decreases the severity of atherosclerosis in apoE deficient mice, possibly through increased expressions of VCAM-1 and monocyte chemotactic protein-1 in the aorta.
authors.affiliation: Department of Clinical Laboratory Medicine, Gifu University School of Medicine, 40 Tsukasa-machi, Gifu 500-8705, Japan.
authors.forename: Hirokazu
authors.initials: H
authors.lastname: Kirii
authors.forename: Tamikazu
authors.initials: T
authors.lastname: Niwa
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Yamada
authors.forename: Hisayasu
authors.initials: H
authors.lastname: Wada
authors.forename: Kuniaki
authors.initials: K
authors.lastname: Saito
authors.forename: Yoichiro
authors.initials: Y
authors.lastname: Iwakura
authors.forename: Masahide
authors.initials: M
authors.lastname: Asano
authors.forename: Hisataka
authors.initials: H
authors.lastname: Moriwaki
authors.forename: Mitsuru
authors.initials: M
authors.lastname: Seishima
mesh_terms: D000818:Animals; D001011:Aorta / Q000378:metabolism; D001024:Aortic Valve Stenosis / Q000097:blood / Q000235:genetics* / Q000473:pathology; D001057:Apolipoproteins E / Q000172:deficiency / Q000502:physiology*; D001161:Arteriosclerosis / Q000097:blood / Q000235:genetics* / Q000473:pathology; D002465:Cell Movement; D018932:Chemokine CCL2 / Q000096:biosynthesis / Q000235:genetics; D005786:Gene Expression Regulation; D007375:Interleukin-1 / Q000172:deficiency / Q000502:physiology*; D008055:Lipids / Q000097:blood; D008264:Macrophages / Q000502:physiology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009000:Monocytes / Q000502:physiology; D012333:RNA, Messenger / Q000096:biosynthesis; D017539:Tunica Intima / Q000473:pathology; D019010:Vascular Cell Adhesion Molecule-1 / Q000096:biosynthesis / Q000235:genetics
chemical_list: D001057:Apolipoproteins E; D018932:Chemokine CCL2; D007375:Interleukin-1; D008055:Lipids; D012333:RNA, Messenger; D019010:Vascular Cell Adhesion Molecule-1