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

BACKGROUND

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.

METHODS

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).

RESULTS

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.

CONCLUSION

MiR-122-5p suppresses cytokine expression in SGBS adipocytes by targeting CPEB1.