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

Dawei Li1, Jinni Chen2, Chuan Yun1

  • 1Department of Endocrinology, The First Affiliated Hospital of Hainan Medical University, Haikou 570102, Hainan, China.

Abstract

Insights

MicroRNA-122-5p (miR-122-5p) suppresses inflammatory cytokine production in childhood obesity by targeting CPEB1. This finding clarifies the role of miR-122-5p in obesity-related inflammation.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Endocrinology

Background:

  • Childhood obesity is linked to inflammation, increasing the risk of related disorders.
  • MicroRNAs (miRNAs) are implicated in the pathogenesis of diseases, including childhood obesity.
  • The specific role of miR-122-5p in childhood obesity remains unclear.

Purpose of the Study:

  • To investigate the function and mechanism of miR-122-5p in childhood obesity.
  • To determine if miR-122-5p affects cytokine expression in adipocytes.

Main Methods:

  • Coculture of Simpson-Golabi-Behmel syndrome (SGBS) adipocytes with macrophages.
  • Assessing cytokine (IL-6, IL-8, MCP-1) expression via RT-qPCR and ELISA.
  • Investigating miR-122-5p and CPEB1 interaction using Western blotting and luciferase assays.

Main Results:

  • Coculture increased pro-inflammatory cytokine expression in SGBS adipocytes.
  • Overexpression of miR-122-5p reduced cytokine levels.
  • miR-122-5p directly targets the 3'-untranslated region of CPEB1, and CPEB1 upregulation rescues the inhibitory effect.

Conclusions:

  • MiR-122-5p acts as a suppressor of cytokine expression in SGBS adipocytes.
  • The mechanism involves direct targeting of cytoplasmic polyadenylation element binding protein 1 (CPEB1).
  • This study elucidates a novel regulatory pathway for inflammation in childhood obesity.

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