Ufm1 inhibits LPS-induced endothelial cell inflammatory responses through the NF-κB signaling pathway

Li,Yuan-Yuan; Zhang,Guang-Ya; He,Jiang-Ping; Zhang,Dan-Dan; Kong,Xiang-Xin; Yuan,Hui-Min; Chen,Feng-Ling

doi:10.3892/ijmm.2017.2947

Ufm1 inhibits LPS-induced endothelial cell inflammatory responses through the NF-κB signaling pathway

Authors:
- Yuan-Yuan Li
- Guang-Ya Zhang
- Jiang-Ping He
- Dan-Dan Zhang
- Xiang-Xin Kong
- Hui-Min Yuan
- Feng-Ling Chen
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Affiliations: Department of Endocrinology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201999, P.R. China
Published online on: April 7, 2017 https://doi.org/10.3892/ijmm.2017.2947
Pages: 1119-1126
Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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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.

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