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LncRNA NEAT1 Regulates Infantile Pneumonia by Sponging miR-146b

Jingjing Cui1, Jian Wang2, Yeke Lv3

  • 1Department of Pediatrics, Guan Grao County Hospital of Traditional Chinese Medicine, Dongying, 257300, Shandong Province, China.

Molecular Biotechnology
|May 12, 2021
PubMed

Insights

Long non-coding RNA NEAT1 is upregulated in infantile pneumonia and sponges miR-146b. Inhibiting NEAT1 or overexpressing miR-146b improves cell viability and reduces apoptosis in pneumonia models.

Area of Science:

  • Molecular Biology
  • Pediatrics
  • Genetics

Background:

  • Infantile pneumonia is a significant respiratory illness in children.
  • Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) are implicated in various diseases, including pneumonia.
  • The specific roles of lncRNA NEAT1 and miR-146b in infantile pneumonia require further elucidation.

Purpose of the Study:

  • To investigate the expression levels of lncRNA NEAT1 and miR-146b in infantile pneumonia.
  • To explore the regulatory relationship between lncRNA NEAT1 and miR-146b in the context of infantile pneumonia.
  • To determine the functional effects of lncRNA NEAT1 and miR-146b on lung fibroblast cells under pneumonia-inducing conditions.

Main Methods:

  • Quantitative real-time PCR (qPCR) was used to measure lncRNA NEAT1 and miR-146b expression in patient serum.
  • A pneumonia model was established using human embryonic lung fibroblasts (HFL1) induced by lipopolysaccharide (LPS).
  • lncRNA NEAT1 inhibition and miR-146b overexpression vectors were transfected into HFL1 cells, followed by assessments of cell viability and apoptosis.
  • Dual-luciferase reporter assays and Starbase predictions were employed to confirm the direct interaction between lncRNA NEAT1 and miR-146b.

Main Results:

  • lncRNA NEAT1 expression was significantly upregulated in the serum of children with infantile pneumonia compared to healthy controls.
  • Knockdown of lncRNA NEAT1 enhanced cell viability and reduced apoptosis in LPS-induced HFL1 cells.
  • miR-146b expression was decreased in infantile pneumonia serum.
  • Overexpression of miR-146b promoted cell viability and decreased apoptosis in LPS-induced HFL1 cells.
  • Dual-luciferase reporter assays confirmed that lncRNA NEAT1 directly binds to and sponges miR-146b.

Conclusions:

  • lncRNA NEAT1 acts as a molecular sponge for miR-146b in infantile pneumonia.
  • The NEAT1/miR-146b axis plays a crucial role in regulating cellular processes relevant to infantile pneumonia pathogenesis.
  • Targeting the lncRNA NEAT1/miR-146b interaction may offer a potential therapeutic strategy for infantile pneumonia.

Keywords:
ApoptosisInfantile pneumoniaLncRNA NEAT1MiR-146bProliferation

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