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Long non-coding RNA MEG3 silencing weakens high glucose-induced mesangial cell injury by decreasing LIN28B expression

Lu Rong1, Huanzhou Xue1, Jianwei Hao1

  • 1Department of Urology, People's Hospital of Zhengzhou University, Henan Provincial People's Hospital, Zhengzhou, China.

Kidney Research and Clinical Practice
|December 26, 2023
PubMed
Abstract

Insights

Diabetic nephropathy (DN) involves long non-coding RNA MEG3 and microRNA-23c. MEG3 impacts kidney cell injury by regulating the miR-23c/LIN28B pathway, offering insights into DN mechanisms.

Area of Science:

  • Molecular Biology
  • Genetics
  • Nephrology

Background:

  • Diabetic nephropathy (DN) is a prevalent kidney complication in diabetes.
  • Long non-coding RNA maternally expressed gene 3 (MEG3) and microRNA-23c are implicated in DN.
  • The precise molecular interplay between MEG3 and miR-23c in DN pathogenesis is not fully understood.

Purpose of the Study:

  • To elucidate the molecular mechanism of MEG3 and miR-23c in diabetic nephropathy.
  • To investigate the role of the MEG3/miR-23c axis in human mesangial cell (HMC) injury under high glucose conditions.

Main Methods:

  • Human mesangial cells (HMCs) were exposed to high glucose (HG) to model DN in vitro.
  • Expression levels of MEG3 and miR-23c were quantified.
  • MEG3 silencing effects on HG-induced HMC injury were assessed.
  • The interaction between MEG3 and miR-23c was validated using dual-luciferase reporter and RNA immunoprecipitation assays.

Main Results:

  • MEG3 was upregulated in DN patient serums and HG-treated HMCs.
  • MEG3 knockdown attenuated HG-induced HMC proliferation, extracellular matrix (ECM) accumulation, and inflammation.
  • MEG3 directly targeted miR-23c, influencing lin-28 homolog B (LIN28B) expression.
  • Inhibition of miR-23c or overexpression of LIN28B partially reversed the protective effects of MEG3 modulation.

Conclusions:

  • MEG3 exacerbates HMC injury in DN by modulating the miR-23c/LIN28B axis.
  • This study clarifies a key molecular pathway underlying MEG3's role in DN.
  • Findings provide a foundation for understanding DN pathogenesis and potential therapeutic targets.
Keywords:
Diabetic nephropathiesGeneticsMEG3 non-coding RNAMIRN23 microRNA

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