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血管生成素-1 可保护 3T3-L1 前脂肪细胞免受饱和脂肪酸诱导的细胞死亡。

Angiopoietin-1 protects 3T3-L1 preadipocytes from saturated fatty acid-induced cell death.

机构信息

Department of Foods & Nutrition, University of Georgia, Athens, GA, USA.

Department of Food Science & Technology, University of Georgia, Athens, GA, USA.

出版信息

Nutr Res. 2020 Apr;76:20-28. doi: 10.1016/j.nutres.2020.02.007. Epub 2020 Feb 13.

DOI:10.1016/j.nutres.2020.02.007
PMID:32146252
Abstract

Cross talk between endothelial cells and adipocytes is vital to adipocyte functions, but little is known about the mechanisms or factors controlling the process. Angiogenesis is a critical component linking the endothelium to healthy adipogenesis, yet it is not known if or how it is involved in adipocyte physiology. Therefore, the purpose of this study was to determine the effect of angiopoietin-1 (Ang-1) and -2 (Ang-2) as well as their receptor, Tie-2, on adipocyte physiology. 3T3-L1 pre- and mature adipocytes were found to express Ang-1, Ang-2, and Tie-2, which decrease upon polyunsaturated fatty acid treatment. Furthermore, 3T3-L1 cells treated with recombinant Ang-1 or Ang-2 increased expression of the antiapoptotic gene Bcl-x and decreased expression of the proapoptotic gene Casp-8. Next, preadipocytes were treated with saturated fatty acids (SFAs) to induce cell stress. SFA-mediated splicing of X-box-binding protein-1 was reduced by co-treatment with Ang-1, and cell viability was improved in the presence of SFAs + Ang-1. Taken together, these results indicate that Ang-1 may protect preadipocytes from SFA-induced apoptosis and endoplasmic reticulum stress.

摘要

内皮细胞和脂肪细胞之间的串扰对于脂肪细胞功能至关重要,但控制该过程的机制或因素知之甚少。血管生成是将内皮细胞与健康的脂肪生成联系起来的关键组成部分,但尚不清楚它是否以及如何参与脂肪细胞的生理学功能。因此,本研究旨在确定血管生成素-1 (Ang-1) 和 -2 (Ang-2) 及其受体 Tie-2 对脂肪细胞生理学的影响。发现 3T3-L1 前体脂肪细胞和成熟脂肪细胞表达 Ang-1、Ang-2 和 Tie-2,而多不饱和脂肪酸处理会使其表达减少。此外,用重组 Ang-1 或 Ang-2 处理的 3T3-L1 细胞增加了抗凋亡基因 Bcl-x 的表达,降低了促凋亡基因 Casp-8 的表达。接下来,用饱和脂肪酸 (SFAs) 处理前体脂肪细胞以诱导细胞应激。Ang-1 的共处理可降低 X 盒结合蛋白-1 的剪接,并且在存在 SFAs+Ang-1 的情况下细胞活力得到改善。综上所述,这些结果表明 Ang-1 可能保护前体脂肪细胞免受 SFA 诱导的细胞凋亡和内质网应激。

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