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Long non-coding RNA MEG3 promotes fibrosis and inflammatory response in diabetic nephropathy via miR-181a/Egr-1/TLR4

Fangfang Zha1, Xiaolu Qu2, Bo Tang1

  • 1Department of Nephrology, Qingpu Branch of Zhongshan Hospital Affiliated to Fudan University, Qingpu District, Shanghai 201700, P.R. China.

Aging
|June 14, 2019
PubMed

Insights

Long non-coding RNA MEG3 exacerbates diabetic nephropathy (DN) by promoting fibrosis and inflammation. It acts as a sponge for miR-181a, regulating the Egr-1/TLR4 pathway in kidney cells.

Area of Science:

  • Molecular Biology
  • Genetics
  • Nephrology

Background:

  • Diabetic nephropathy (DN) is a severe complication of diabetes.
  • Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in DN pathogenesis.
  • Understanding specific lncRNAs like MEG3 is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the role of long non-coding RNA MEG3 in diabetic nephropathy (DN).
  • To elucidate the molecular mechanisms underlying MEG3's function in DN.
  • To explore the interaction between MEG3, miR-181a, and the Egr-1/TLR4 signaling pathway.

Main Methods:

  • In vivo and in vitro models of diabetic nephropathy.
  • Quantitative real-time PCR to measure MEG3 and miR-181a expression.
  • Western blotting to assess protein levels (Egr-1, TLR4).
  • RNA immunoprecipitation assays to confirm Ago2-dependent interactions.

Main Results:

  • MEG3 expression was significantly upregulated in DN models.
  • MEG3 overexpression enhanced fibrosis and inflammatory responses in mesangial cells.
  • MEG3 acted as an endogenous sponge for miR-181a, inhibiting its function.
  • MiR-181a directly targeted Egr-1, and its inhibition promoted DN-related cellular changes.
  • MEG3 promoted DN progression via the miR-181a/Egr-1/TLR4 signaling axis.

Conclusions:

  • MEG3 plays a pro-fibrotic and pro-inflammatory role in diabetic nephropathy.
  • The MEG3/miR-181a/Egr-1/TLR4 axis represents a novel regulatory pathway in DN.
  • Targeting MEG3 or its downstream effectors may offer therapeutic strategies for DN.
Keywords:
ceRNAdiabetic nephropathylncRNA MEG3miR-181a

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