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CXCL5 inhibits excessive oxidative stress by regulating white adipocyte differentiation

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dc.contributor.authorLee, Dabin-
dc.contributor.authorLee, Kang-Hoon-
dc.contributor.authorKim, Dong Wook-
dc.contributor.authorYoon, Sanghyuk-
dc.contributor.authorCho, Je-Yoel-
dc.date.accessioned2022-09-30T05:58:07Z-
dc.date.available2022-09-30T05:58:07Z-
dc.date.created2022-07-11-
dc.date.issued2022-08-
dc.identifier.citationRedox Biology, Vol.54, p. 102359-
dc.identifier.issn2213-2317-
dc.identifier.urihttps://hdl.handle.net/10371/185045-
dc.description.abstractChemokines 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.-
dc.language영어-
dc.publisherElsevier BV-
dc.titleCXCL5 inhibits excessive oxidative stress by regulating white adipocyte differentiation-
dc.typeArticle-
dc.identifier.doi10.1016/j.redox.2022.102359-
dc.citation.journaltitleRedox Biology-
dc.identifier.wosid000811997200004-
dc.identifier.scopusid2-s2.0-85132221101-
dc.citation.startpage102359-
dc.citation.volume54-
dc.description.isOpenAccessN-
dc.contributor.affiliatedAuthorCho, Je-Yoel-
dc.type.docTypeArticle-
dc.description.journalClass1-
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