MiR-874-3p suppresses TNF-α-induced inflammation in adipocytes by targeting nucleolin

Xingxiang Xu1, Xiaomei Fu2

  • 1Department of Pediatrics, Jurong City People's Hospital, No. 66, Ersheng Road, Jurong, 212400, Jiangsu, China. xxx19820709@sohu.com.

PubMed

Insights

MicroRNA-874-3p, downregulated in obese children, protects against inflammation. It reduces tumor necrosis factor-alpha effects in fat cells by targeting nucleolin and inhibiting NF-kappaB signaling.

Area of Science:

  • Molecular Biology
  • Biochemistry
  • Cell Biology

Background:

  • MicroRNAs (miRNAs) are investigated as biomarkers for early childhood obesity.
  • MiR-874-3p is downregulated in overweight/obese children, but its role is unclear.

Purpose of the Study:

  • To elucidate the function and mechanism of miR-874-3p in childhood obesity progression.
  • To investigate the role of miR-874-3p in tumor necrosis factor-alpha (TNF-α)-induced inflammation in adipocytes.

Main Methods:

  • Established an in vitro cell model using human Simpson-Golabi-Behmel syndrome (SGBS) adipocytes stimulated with TNF-α.
  • Assessed cell viability (CCK-8 assay), proinflammatory cytokines (ELISA), miR-874-3p expression (RT-qPCR), and protein levels (Western blotting).
  • Verified the interaction between miR-874-3p and nucleolin (NCL) using a luciferase reporter assay.

Main Results:

  • Overexpression of miR-874-3p counteracted TNF-α-induced inhibition of cell viability and reduced proinflammatory cytokine production.
  • Nucleolin (NCL) was identified as a direct target of miR-874-3p.
  • miR-874-3p inactivated NCL-mediated nuclear factor kappa B (NF-κB) signaling, and NCL upregulation reversed the effects of miR-874-3p overexpression.

Conclusions:

  • MiR-874-3p plays a protective role against TNF-α-induced inflammation in SGBS adipocytes.
  • The mechanism involves the downregulation of NCL and subsequent inactivation of NF-κB signaling.
  • MiR-874-3p holds potential as a therapeutic target for childhood obesity-related inflammation.

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