title: [Anti-β2GPI antibody promotes release of inflammatory and pro-thrombosis molecules from arteries in apolipoprotein E-deficient mice].
abstract: Objective To investigate the roles of anti-beta 2 glycoprotein I antibodies (anti-β2GPI Ab) in the expressions of atherosclerosis(AS)-related inflammatory factors and pro-thrombosis molecules in apolipoprotein E-deficient (ApoE-/-) mice. Methods ApoE-/-mice were randomly divided into normal saline (NS) group, 100 μg anti-β2GPI Ab group, 100 μg homologous antibody (rabbit-IgG) group and 100 μg β2GPI/anti-β2GPI Ab complex group after silastic collars were placed around their carotid arteries by surgery. All mice were fed a high fat diet and corresponding stimuli were given through intraperitoneal injection at 7-day intervals. Six weeks later, the mice were executed. The blockage of carotid arteries of the operated side was observed by HE staining. The expressions of TLR4, tissue factor (TF) and von Willebrand factor (vWF) were detected by immunohistochemistry. The mRNA levels of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in aorta were tested by real-time quantitative PCR. Results HE staining showed that the blockage of carotid arteries in antibody group was the most obvious. The immunohistochemistry showed that the expressions of TLR4, TF and vWF in anti-β2GPI Ab group increased remarkably. Furthermore, the mRNA levels of IL-1β and TNF-α in anti-β2GPI Ab group were higher than those in the other groups. Conclusion The anti-β2GPI antibody promotes the formation of atherosclerotic plaques in mice by up-regulating the release of inflammatory cytokines IL-1β, TNF-α and thrombosis-related molecules TF, vWF and TLR4, ultimately enhancing the development of AS.
authors.affiliation: School of Medicine, Jiangsu University, Zhenjiang 212013, China.
authors.forename: Xiaojie
authors.initials: X
authors.lastname: Zhu
authors.affiliation: School of Medicine, Jiangsu University, Zhenjiang 212013, China. *Corresponding author, E-mail: hongzhou0123@163.com.
authors.forename: Hong
authors.initials: H
authors.lastname: Zhou
authors.affiliation: School of Medicine, Jiangsu University, Zhenjiang 212013, China.
authors.forename: Xiaoyan
authors.initials: X
authors.lastname: Wang
authors.affiliation: School of Medicine, Jiangsu University, Zhenjiang 212013, China.
authors.forename: Qianqian
authors.initials: Q
authors.lastname: Cai
authors.affiliation: School of Medicine, Jiangsu University, Zhenjiang 212013, China.
authors.forename: Chao
authors.initials: C
authors.lastname: He
authors.affiliation: School of Medicine, Jiangsu University, Zhenjiang 212013, China.
authors.forename: Longfei
authors.initials: L
authors.lastname: Xia
authors.affiliation: School of Medicine, Jiangsu University, Zhenjiang 212013, China.
authors.forename: Guiting
authors.initials: G
authors.lastname: Zhang
authors.affiliation: School of Medicine, Jiangsu University, Zhenjiang 212013, China.
authors.forename: Hang
authors.initials: H
authors.lastname: Ouyang
mesh_terms: D000818:Animals; D000906:Antibodies / Q000008:administration & dosage* / Q000009:adverse effects; D001057:Apolipoproteins E / Q000172:deficiency* / Q000235:genetics; D001158:Arteries / Q000187:drug effects / Q000378:metabolism*; D050197:Atherosclerosis / Q000209:etiology / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D013925:Thromboplastin / Q000235:genetics / Q000378:metabolism; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism; D053482:beta 2-Glycoprotein I / Q000276:immunology*; D014841:von Willebrand Factor / Q000235:genetics / Q000378:metabolism
chemical_list: D000906:Antibodies; D001057:Apolipoproteins E; D053583:Interleukin-1beta; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; D053482:beta 2-Glycoprotein I; D014841:von Willebrand Factor; D013925:Thromboplastin