MiR-122–5p regulates the pathogenesis of childhood obesity by targeting CPEB1

小RNA 下调和上调 油红O 炎症 细胞因子 分子生物学 发病机制 化学 生物 脂肪组织 内分泌学 基因 免疫学 生物化学 脂肪生成
作者
Dawei Li,Jinni Chen,Chuan Yun,Xiaoyan Li,Zhenzhen Huang
出处
期刊:Obesity Research & Clinical Practice [Elsevier BV]
卷期号:16 (3): 206-213 被引量:3
标识
DOI:10.1016/j.orcp.2022.05.006
摘要

Childhood obesity is strongly associated with inflammation which contributes to the development of several obesity-related disorders. Accumulating evidence has suggested that microRNAs (miRNAs) are involved in the pathogenesis of multiple human diseases, including childhood obesity. MiR-122-5p was reported to be related to obesity in childhood, however, the detailed function and mechanism of miR-122-5p are still obscure.Simpson-Golabi-Behmel syndrome (SGBS) adipocytes were cocultured with macrophage cell line THP-1 or macrophage-conditioned medium (MacCM) to promote cytokine expression. Oil Red O staining was used to detect the accumulation of lipid droplets in SGBS cells. The expression of interleukin 6 (IL-6), IL-8, and monocyte chemoattractant protein 1 (MCP-1) at mRNA and protein levels was assessed by RT-qPCR and ELISA, respectively. Western blotting was used for measuring protein levels of target genes of miR-122-5p. The luciferase reporter assay was applied for detecting the binding relation between miR-122-5p and cytoplasmic polyadenylation element binding protein 1 (CPEB1).Coculture of SGBS adipocytes and THP-1 macrophages/MacCM promoted IL-6, IL-8, and MCP-1 expression at mRNA and protein levels. Overexpression of miR-122-5p inhibited IL-6, IL-8, and MCP-1 expression in SGBS adipocytes, and this inhibitory effect was rescued by CPEB1 upregulation. CPEB1 3'-untranslated region was directly targeted by miR-122-5p.MiR-122-5p suppresses cytokine expression in SGBS adipocytes by targeting CPEB1.

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