Secreted Frizzled-Related Protein 5 Mediates Wnt5a Expression in Microcystin-Leucine-Arginine-Induced Liver Lipid Metabolism Disorder in Mice.

Mei Yan Yang, Fu Rong Yu, Qian Qian Ji, Hui Ying Zhang, Jia Xiang Zhang, Dao Jun Chen
{"title":"Secreted Frizzled-Related Protein 5 Mediates Wnt5a Expression in Microcystin-Leucine-Arginine-Induced Liver Lipid Metabolism Disorder in Mice.","authors":"Mei Yan Yang, Fu Rong Yu, Qian Qian Ji, Hui Ying Zhang, Jia Xiang Zhang, Dao Jun Chen","doi":"10.3967/bes2024.081","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>Microcystin-leucine-arginine (MC-LR) exposure induces lipid metabolism disorders in the liver. Secreted frizzled-related protein 5 (SFRP5) is a natural antagonist of winglesstype MMTV integration site family, member 5A (Wnt5a) and an anti-inflammatory adipocytokine. In this study, we aimed to investigate whether MC-LR can induce lipid metabolism disorders in hepatocytes and whether SFRP5, which has anti-inflammatory effects, can alleviate the effects of hepatic lipid metabolism by inhibiting the Wnt5a/Jun N-terminal kinase (JNK) pathway.</p><p><strong>Methods: </strong>We exposed mice to MC-LR <i>in vivo</i> to induce liver lipid metabolism disorders. Subsequently, mouse hepatocytes that overexpressed SFRP5 or did not express SFRP5 were exposed to MC-LR, and the effects of SFRP5 overexpression on inflammation and Wnt5a/JNK activation by MC-LR were observed.</p><p><strong>Results: </strong>MC-LR exposure induced liver lipid metabolism disorders in mice and significantly decreased SFRP5 mRNA and protein levels in a concentration-dependent manner. SFRP5 overexpression in AML12 cells suppressed MC-LR-induced inflammation. Overexpression of SFRP5 also inhibited Wnt5a and phosphorylation of JNK.</p><p><strong>Conclusion: </strong>MC-LR can induce lipid metabolism disorders in mice, and SFRP5 can attenuate lipid metabolism disorders in the mouse liver by inhibiting Wnt5a/JNK signaling.</p>","PeriodicalId":93903,"journal":{"name":"Biomedical and environmental sciences : BES","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2024-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biomedical and environmental sciences : BES","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3967/bes2024.081","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Objective: Microcystin-leucine-arginine (MC-LR) exposure induces lipid metabolism disorders in the liver. Secreted frizzled-related protein 5 (SFRP5) is a natural antagonist of winglesstype MMTV integration site family, member 5A (Wnt5a) and an anti-inflammatory adipocytokine. In this study, we aimed to investigate whether MC-LR can induce lipid metabolism disorders in hepatocytes and whether SFRP5, which has anti-inflammatory effects, can alleviate the effects of hepatic lipid metabolism by inhibiting the Wnt5a/Jun N-terminal kinase (JNK) pathway.

Methods: We exposed mice to MC-LR in vivo to induce liver lipid metabolism disorders. Subsequently, mouse hepatocytes that overexpressed SFRP5 or did not express SFRP5 were exposed to MC-LR, and the effects of SFRP5 overexpression on inflammation and Wnt5a/JNK activation by MC-LR were observed.

Results: MC-LR exposure induced liver lipid metabolism disorders in mice and significantly decreased SFRP5 mRNA and protein levels in a concentration-dependent manner. SFRP5 overexpression in AML12 cells suppressed MC-LR-induced inflammation. Overexpression of SFRP5 also inhibited Wnt5a and phosphorylation of JNK.

Conclusion: MC-LR can induce lipid metabolism disorders in mice, and SFRP5 can attenuate lipid metabolism disorders in the mouse liver by inhibiting Wnt5a/JNK signaling.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
分泌型Frizzled相关蛋白5在微囊藻-亮氨酸-精氨酸诱导的小鼠肝脂代谢紊乱中介导Wnt5a的表达
目的微囊藻毒素-亮氨酸-精氨酸(MC-LR)暴露会诱发肝脏脂质代谢紊乱。分泌的褐飞虱相关蛋白 5(SFRP5)是翼型 MMTV 整合位点家族 5A 成员(Wnt5a)的天然拮抗剂,也是一种抗炎性脂肪细胞因子。本研究旨在探讨 MC-LR 是否能诱导肝细胞脂质代谢紊乱,以及具有抗炎作用的 SFRP5 是否能通过抑制 Wnt5a/Jun N-terminal kinase(JNK)通路减轻肝脂质代谢紊乱的影响:方法:我们让小鼠体内暴露于 MC-LR 以诱导肝脏脂质代谢紊乱。随后,将过表达或不表达 SFRP5 的小鼠肝细胞暴露于 MC-LR,观察 SFRP5 过表达对 MC-LR 引起的炎症和 Wnt5a/JNK 激活的影响:结果:暴露于MC-LR会诱发小鼠肝脏脂质代谢紊乱,并以浓度依赖性方式显著降低SFRP5 mRNA和蛋白水平。在 AML12 细胞中过表达 SFRP5 可抑制 MC-LR 诱导的炎症。过表达 SFRP5 还能抑制 Wnt5a 和 JNK 的磷酸化:结论:MC-LR可诱导小鼠脂质代谢紊乱,而SFRP5可通过抑制Wnt5a/JNK信号转导减轻小鼠肝脏脂质代谢紊乱。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
Association between Exposure of Rare Earth Elements and Outcomes of In Vitro Fertilization-Embryo Transfer in Beijing. ATM Activation is Key in Vasculogenic Mimicry Formation by Glioma Stem-like Cells. Changes on Stroke Burden Attributable to Ambient Fine Particulate Matter in China. Effects of Curcumin on Neuroinflammation and the Nrf2/HO-1 Pathway in Rat Brains Following Gas Explosion. Health Risk Assessment of Employees Exposed to Chlorination By-products of Recreational Water in Large Amusement Parks in Shanghai.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1