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Transcription Factor p300 Regulated miR-451b Weakens the Cigarette Smoke Extract-Induced Cellular Stress by Targeting

Wen Shen1, Shukun Wang1, Ruili Wang1

  • 1Department of Respiratory Medicine, The Second Affiliated Hospital of Kunming Medical University, Kunming, China.

Oxidative Medicine and Cellular Longevity
|October 24, 2022
PubMed
Abstract

Insights

MicroRNA-451b (miR-451b) may protect against chronic obstructive pulmonary disease (COPD) by downregulating the RhoA/ROCK2 pathway. This study investigates its role in cigarette smoke-induced lung damage.

Area of Science:

  • Pulmonary Medicine
  • Molecular Biology
  • Biochemistry

Background:

  • Chronic obstructive pulmonary disease (COPD) pathogenesis involves complex molecular mechanisms.
  • MicroRNA-451b (miR-451b) has been proposed as a potential biomarker in smokers with or without COPD.
  • The precise function and molecular pathways of miR-451b in COPD remain unclear.

Purpose of the Study:

  • To elucidate the functional role and molecular mechanisms of miR-451b in cigarette smoke extract (CSE)-induced lung injury.
  • To investigate the relationship between p300, miR-451b, and RhoA in the context of COPD pathogenesis.
  • To determine the therapeutic potential of miR-451b in mitigating CSE-induced cellular stress.

Main Methods:

  • Macrophages and lung fibroblasts were treated with cigarette smoke extract (CSE).
  • Expression levels of miR-451b, p300, and RhoA were quantified.
  • Luciferase reporter assays validated gene targets, while ELISA and Western blotting assessed protein and cytokine release and collagen production.

Main Results:

  • CSE exposure downregulated p300 and miR-451b while upregulating RhoA.
  • RhoA was identified as a direct target gene of miR-451b.
  • Overexpression of miR-451b reduced inflammatory cytokine release (IL-12, TNF-α), suppressed RhoA/ROCK2 pathway activation, and inhibited cell migration and invasion.

Conclusions:

  • The p300/miR-451b axis plays a protective role against CSE-induced cellular stress in COPD.
  • Downregulation of the RhoA/ROCK2 pathway by miR-451b is a key mechanism in this protective effect.
  • miR-451b represents a potential therapeutic target for managing COPD.

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