title: Inhibition of siglec-1 by lentivirus mediated small interfering RNA attenuates atherogenesis in apoE-deficient mice.
abstract: Siglec-1 is highly expressed on circulating monocytes and plaque macrophages in atherosclerotic patients, but the exact role of Siglec-1 in atherosclerosis has not been elucidated.
  
  
  
  Lentiviral vector containing small interfering RNA targeting Siglec-1 (Lv-shSiglec-1) or control vector (Lv-shNC) were injected intravenously into 6-week old Apoe-/-mice. Then onset of atherosclerosis was observed.
  
  
  
  Siglec-1 was highly expressed in aortic plaques and it can be down-regulated by Lv-shSiglec-1 injection. The plaque area and serum pro-inflammatory cytokine (IL-1β, IL-6, TNF-α and IL-17A) levels in Lv-shSiglec-1 mice were significantly lower than Lv-shNC mice, whereas IL-10 was higher. Moreover, plaque macrophages accumulation in aortic wall in Lv-shSiglec-1 mice was diminish, partly by decreased secretion of MCP-1/CXCL2 and CCR2/CXCR2 of aortas and monocytes, respectively. Furthermore, silencing of Siglec-1 can attenuate oxLDL uptake by peritoneal macrophages.
  
  
  
  Inhibition of Siglec-1 can prevent atherosclerotic lesion formation by suppress monocytes-endothelial cells adhesion and macrophages accumulation.
authors.affiliation: Department of Laboratory Medicine, Chengdu Military General Hospital, Chengdu, China. Electronic address: xys10@163.com.
authors.forename: Yi-Song
authors.initials: YS
authors.lastname: Xiong
authors.affiliation: Department of Laboratory Medicine, Chengdu Military General Hospital, Chengdu, China.
authors.forename: Ai-Lin
authors.initials: AL
authors.lastname: Wu
authors.affiliation: Department of Gastroenterology, Chengdu Military General Hospital, Chengdu, China.
authors.forename: Dong
authors.initials: D
authors.lastname: Mu
authors.affiliation: Center of Laboratory Medicine, Affiliated Hospital, Nantong University, Nantong, China; Institute of Public Health, Nantong University, Nantong, China.
authors.forename: Juan
authors.initials: J
authors.lastname: Yu
authors.affiliation: Department of Laboratory Medicine, Chengdu Military General Hospital, Chengdu, China.
authors.forename: Ping
authors.initials: P
authors.lastname: Zeng
authors.affiliation: Department of Laboratory Diagnostics, Changhai Hospital, Second Military Medical University, Shanghai, China.
authors.forename: Yi
authors.initials: Y
authors.lastname: Sun
authors.affiliation: Department of Laboratory Medicine, Chengdu Military General Hospital, Chengdu, China. Electronic address: jxiong007@126.com.
authors.forename: Jie
authors.initials: J
authors.lastname: Xiong
mesh_terms: D000818:Animals; D001011:Aorta / Q000276:immunology / Q000473:pathology; D001057:Apolipoproteins E / Q000235:genetics; D050197:Atherosclerosis / Q000235:genetics / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D016207:Cytokines / Q000097:blood; D016086:Lentivirus / Q000235:genetics; D008055:Lipids / Q000097:blood; D008264:Macrophages / Q000378:metabolism; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D009000:Monocytes / Q000378:metabolism; D034741:RNA, Small Interfering / Q000235:genetics; D063267:Sialic Acid Binding Ig-like Lectin 1 / Q000235:genetics*
chemical_list: D001057:Apolipoproteins E; D016207:Cytokines; D008055:Lipids; D034741:RNA, Small Interfering; D063267:Sialic Acid Binding Ig-like Lectin 1; C571167:Siglec1 protein, mouse
keywords: Atherosclerosis; Cell adhesion molecules; Gene therapy; Inflammation