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The long noncoding RNA Meg3 mediates TLR4-induced inflammation in experimental obstructive nephropathy.

Wai Han Yiu1, Sarah W Y Lok1, Rui Xue1

  • 1Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong.

Clinical Science (London, England : 1979)
|January 27, 2023
PubMed
Summary

Long noncoding RNA Meg3 promotes kidney inflammation and fibrosis in chronic kidney disease (CKD). Targeting Meg3 may offer a novel therapeutic strategy for TLR4-driven kidney injury.

Keywords:
Meg3TLR4 signalingkidney fibrosislarge intervening non-coding RNAtubular injury

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Area of Science:

  • Nephrology
  • Molecular Biology
  • Immunology

Background:

  • Kidney inflammation drives chronic kidney disease (CKD) progression.
  • Toll-like receptor 4 (TLR4) signaling is implicated in kidney inflammation, but its regulatory mechanisms in tubular injury remain unclear.

Purpose of the Study:

  • To investigate the role of long noncoding RNA (lncRNA) Meg3 in TLR4-mediated kidney inflammation and fibrosis.
  • To elucidate the regulatory pathway involving Meg3 in tubular epithelial cells during kidney injury.

Main Methods:

  • Utilized tubule-specific TLR4 knockout mice to study obstruction-induced kidney injury.
  • Performed transcriptome analysis to identify differentially expressed lncRNAs.
  • Investigated Meg3 induction by lipopolysaccharide (LPS) in tubular epithelial cells via a p53-dependent pathway.
  • Assessed the effects of Meg3 silencing on inflammatory responses and kidney fibrosis in vitro and in vivo.

Main Results:

  • Tubule-specific deletion of TLR4 protected against kidney injury, reducing inflammation, macrophage infiltration, and fibrosis.
  • lncRNA Meg3 was significantly downregulated in the kidneys of TLR4 knockout mice.
  • Meg3 expression was induced by LPS in tubular cells through p53 signaling.
  • Meg3 silencing attenuated LPS-induced cytokine production (CCL-2, CXCL-2) and p38 MAPK activation, and ameliorated kidney fibrosis.

Conclusions:

  • lncRNA Meg3 plays a pro-inflammatory role in the progression of chronic kidney disease.
  • A novel regulatory pathway involving TLR4, p53, and Meg3 in tubular epithelial cells contributes to kidney inflammation and fibrosis.
  • Targeting lncRNA Meg3 represents a potential therapeutic strategy for TLR4-driven kidney diseases.