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miR-26a-5p mediates TLR signaling pathway by targeting CTGF in LPS-induced alveolar macrophage

Chunyan Li1, Tingfeng Han2, Run Li1

  • 1Department of Emergency, Luoyang Central Hospital Affiliated to Zhengzhou University, Luoyang 471000, He'nan Province, China.

Bioscience Reports
|May 19, 2020
PubMed

Insights

MicroRNA-26a-5p (miR-26a-5p) inhibits connective tissue growth factor (CTGF) in severe pneumonia models. This mechanism reduces inflammation and cell apoptosis in alveolar macrophages.

Area of Science:

  • Molecular Biology
  • Immunology
  • Cell Biology

Background:

  • Severe pneumonia involves complex cellular responses in alveolar macrophages.
  • Understanding the regulatory mechanisms of microRNAs and growth factors is crucial for pneumonia research.

Purpose of the Study:

  • To investigate the regulatory roles of miR-26a-5p and connective tissue growth factor (CTGF) in lipopolysaccharide (LPS)-induced alveolar macrophages.
  • To elucidate the involvement of the Toll-like receptor (TLR) signaling pathway.

Main Methods:

  • Utilized MH-S cells stimulated with LPS to create a severe pneumonia model.
  • Quantified gene and protein expression of miR-26a-5p, CTGF, TLR2, TLR4, and NF-κB p65 using qRT-PCR and Western Blot.
  • Assessed cell viability and apoptosis via MTT assay and flow cytometry.

Main Results:

  • LPS induction decreased miR-26a-5p expression while increasing CTGF levels.
  • Overexpression of miR-26a-5p enhanced cell viability, reduced apoptosis, and downregulated TLR signaling molecules and pro-inflammatory cytokines (TNF-α, IL-6, IL-1β).
  • CTGF overexpression exhibited opposite effects compared to miR-26a-5p overexpression.

Conclusions:

  • miR-26a-5p suppresses CTGF expression in a severe pneumonia cell model.
  • miR-26a-5p regulates the TLR signaling pathway, inhibiting cell apoptosis and pro-inflammatory cytokine release in alveolar macrophages.
Keywords:
connective tissue growth factormiR-26a-5psevere pneumoniatoll-like receptor signaling pathway

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