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CXCL5 通过调节白色脂肪细胞分化来抑制过度的氧化应激。

CXCL5 inhibits excessive oxidative stress by regulating white adipocyte differentiation.

机构信息

Department of Biochemistry, BK21 Plus and Research Institute for Veterinary Science, College of Veterinary Medicine, Seoul National University, Seoul, 08826, Republic of Korea; Comparative Medicine Disease Research Center, Seoul National University, Seoul, 08826, Republic of Korea.

Department of Biochemistry, BK21 Plus and Research Institute for Veterinary Science, College of Veterinary Medicine, Seoul National University, Seoul, 08826, Republic of Korea.

出版信息

Redox Biol. 2022 Aug;54:102359. doi: 10.1016/j.redox.2022.102359. Epub 2022 Jun 3.

DOI:10.1016/j.redox.2022.102359
PMID:35696764
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9194457/
Abstract

Chemokines have been well-documented as a major factor in immune cell migration and the regulation of immune responses. However, recent studies have reported that chemokines have diverse roles, both in immune cells and other cell types, including adipocytes. This study investigated the molecular functions of C-X-C motif chemokine ligand 5 (CXCL5) in white adipose cells using Cxcl5 knock-out (KO) mice fed a high-fat diet (HFD). The expression of Cxcl5 decreased by 90% during adipocyte differentiation and remained at a low level in mature adipocytes. Moreover, adipogenesis was enhanced when adipocytes were differentiated from the stromal vascular fraction (SFV) of Cxcl5 KO mice. Feeding an HFD increased the generation of reactive oxygen species (ROS) and promoted abnormal adipogenesis in Cxcl5 KO mice. Oxidative stress and insulin resistance occurred in Cxcl5 KO mice due to decreased antioxidant enzymes and failure to remove ROS. These results indicate the principal roles of CXCL5 in adipogenesis and ROS regulation in adipose tissue, further suggesting that CXCL5 is a valuable chemokine for metabolic disease research.

摘要

趋化因子已被充分证明是免疫细胞迁移和免疫反应调节的主要因素。然而,最近的研究报告称,趋化因子在免疫细胞和其他细胞类型(包括脂肪细胞)中具有多种作用。本研究使用高脂肪饮食(HFD)喂养的 Cxcl5 敲除(KO)小鼠,研究了 C-X-C 基序趋化因子配体 5(CXCL5)在白色脂肪细胞中的分子功能。在脂肪细胞分化过程中,Cxcl5 的表达降低了 90%,在成熟脂肪细胞中仍保持低水平。此外,当从 Cxcl5 KO 小鼠的基质血管部分(SFV)分化出脂肪细胞时,脂肪生成得到增强。喂食 HFD 会增加活性氧(ROS)的产生,并促进 Cxcl5 KO 小鼠异常的脂肪生成。由于抗氧化酶减少和不能清除 ROS,Cxcl5 KO 小鼠发生氧化应激和胰岛素抵抗。这些结果表明 CXCL5 在脂肪生成和 ROS 调节中的主要作用,进一步表明 CXCL5 是代谢性疾病研究的有价值的趋化因子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6ef/9194457/26501ddb0c81/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6ef/9194457/4e733ab1ad65/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6ef/9194457/bf7a7bcdbd2b/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6ef/9194457/269b5d1e1b11/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6ef/9194457/49d8e44cd7a7/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6ef/9194457/243f41e9b63e/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6ef/9194457/384ba794ef61/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6ef/9194457/26501ddb0c81/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6ef/9194457/4e733ab1ad65/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6ef/9194457/bf7a7bcdbd2b/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6ef/9194457/269b5d1e1b11/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6ef/9194457/49d8e44cd7a7/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6ef/9194457/243f41e9b63e/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6ef/9194457/384ba794ef61/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6ef/9194457/26501ddb0c81/gr6.jpg

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