title: Ufm1 inhibits LPS-induced endothelial cell inflammatory responses through the NF-κB signaling pathway.
abstract: Endothelial cell dysfunction and inflammatory responses are important early contributors to the occurrence and development of atherosclerosis (AS), which still remains to be decoded. Ubiquitin-fold modifier 1 (Ufm1) is a new member of the ubiquitin-like protein family, and its biological function remains largely unknown, particularly in endothelial cell injury and inflammatory responses. In the present study, we showed that Ufm1 was highly expressed in both the nucleus and cytoplasm of human umbilical vein endothelial cells (HUVECs). We also demonstrated that the Ufm1 expression level was increased following lipopolysaccharide (LPS)‑induced inflammation in HUVECs. Moreover, overexpression of Ufm1 in HUVECs alleviated the inflammatory responses induced by LPS treatment. Additionally, we found that Ufm1 overexpression inhibited the nuclear translocation of nuclear factor-κB (NF-κB) after LPS treatment, suggesting its implication in the LPS/Toll-like receptor 4 (TLR4)/NF-κB pathway. Taken together, in addition to decoding its expression pattern in endothelial cells, we showed for the first time that Ufm1 is upregulated in LPS-induced inflammation and Ufm1 plays an inhibitory role in inflammatory responses by targeting NF-κB nuclear translocation. Thus, Ufm1 may be a novel gene that protects against inflammatory responses.
authors.affiliation: Department of Endocrinology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201999, P.R. China.
authors.forename: Yuan-Yuan
authors.initials: YY
authors.lastname: Li
authors.affiliation: Department of Endocrinology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201999, P.R. China.
authors.forename: Guang-Ya
authors.initials: GY
authors.lastname: Zhang
authors.affiliation: Department of Endocrinology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201999, P.R. China.
authors.forename: Jiang-Ping
authors.initials: JP
authors.lastname: He
authors.affiliation: Department of Endocrinology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201999, P.R. China.
authors.forename: Dan-Dan
authors.initials: DD
authors.lastname: Zhang
authors.affiliation: Department of Endocrinology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201999, P.R. China.
authors.forename: Xiang-Xin
authors.initials: XX
authors.lastname: Kong
authors.affiliation: Department of Endocrinology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201999, P.R. China.
authors.forename: Hui-Min
authors.initials: HM
authors.lastname: Yuan
authors.affiliation: Department of Endocrinology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201999, P.R. China.
authors.forename: Feng-Ling
authors.initials: FL
authors.lastname: Chen
mesh_terms: D016207:Cytokines / Q000378:metabolism; D042783:Endothelial Cells / Q000378:metabolism*; D015870:Gene Expression; D061307:Human Umbilical Vein Endothelial Cells; D006801:Humans; D007249:Inflammation / Q000209:etiology* / Q000378:metabolism*; D018836:Inflammation Mediators / Q000378:metabolism; D008070:Lipopolysaccharides / Q000009:adverse effects; D008954:Models, Biological; D016328:NF-kappa B / Q000378:metabolism*; D011506:Proteins / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D016328:NF-kappa B; D011506:Proteins; D012333:RNA, Messenger; C502094:UFM1 protein, human