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- Title
Nesfatin-1 inhibits free fatty acid ( FFA )-induced endothelial inflammation via Gfi1/NF-κB signaling.
- Authors
Qingtao Meng; Qin Lu; Zhipeng Zhang; Jiyi Liu; Yu Lou; Yuwei Wang; Jihong Liu
- Abstract
Nesfatin-1 is a neuropeptide produced in the hypothalamus. It is known that Nesfatin-1 is involved in food uptake, fat storage, and other metabolic regulation. We hypothesized that Nesfatin-1 may play a role in cardiovascular tissue. Free fatty acids (FFAs) are known to be the risk factor for cardiovascular diseases. FFA-mediated endothelial dysfunction is the critical mechanism of many cardiovascular disorders. The present study explores the protective effects of Nesfatin-1 on FFA-induced endothelial inflammation and the underlying mechanism. We found that significantly increased lactate dehydrogenase release and production of inflammatory factors were observed in FFA-treated human aortic endothelial cells (HAECs), accompanied by the enhanced attachment of U937 monocytes to HAECs and upregulated cell adhesion molecule vascular cell adhesion molecule-1, which were dramatically reversed by the treatment with Nesfatin-1. In addition, the promoted level of nuclear regulator NF-κB p65 and transcriptional function of NF-κB in FFA-treated HAECs were greatly suppressed by HAECs. Growth Factor Independent 1 Transcriptional Repressor 1 (Gfi1), an important negative regulator of NF-κB activity, was significantly downregulated in HAECs by FFAs and was upregulated by Nesfatin-1. Lastly, the inhibitory effects of Nesfatin-1 against FFA-induced NF-κB activation and adhesion of U937 monocytes to HAECs were abolished by the knockdown of Gfi1. In conclusion, our data reveal that Nesfatin-1 inhibited FFA-induced endothelial inflammation mediated by the Gfi1/NF-κB signaling pathway.
- Subjects
FREE fatty acids; CELL adhesion molecules; DISEASE risk factors; VASCULAR cell adhesion molecule-1; METABOLIC regulation; LACTATE dehydrogenase; CELL adhesion; HYPOTHALAMUS
- Publication
Bioscience, Biotechnology & Biochemistry, 2022, Vol 86, Issue 1, p47
- ISSN
0916-8451
- Publication type
Article
- DOI
10.1093/bbb/zbab186