التفاصيل البيبلوغرافية
| العنوان: |
Nesfatin-1 inhibits free fatty acid ( FFA )-induced endothelial inflammation via Gfi1/NF-κB signaling. |
| المؤلفون: |
Qingtao Meng, Qin Lu, Zhipeng Zhang, Jiyi Liu, Yu Lou, Yuwei Wang, Jihong Liu |
| المصدر: |
Bioscience, Biotechnology & Biochemistry; Jan2022, Vol. 86 Issue 1, p47-55, 9p |
| مصطلحات موضوعية: |
FREE fatty acids, CELL adhesion molecules, DISEASE risk factors, VASCULAR cell adhesion molecule-1, METABOLIC regulation, LACTATE dehydrogenase, CELL adhesion, HYPOTHALAMUS |
| مستخلص: |
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. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
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