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Hedgehog signaling modulates cigarette-induced COPD development.

Fang Ying Lu1,2, Rong Chen1,2, Min Zhou1,2

  • 1Department of Respiratory and Critical Care Medicine, Shanghai Rui Jin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200025, P.R. China.

Experimental and Therapeutic Medicine
|May 19, 2021
PubMed
Summary
This summary is machine-generated.

Hedgehog (Hh) signaling disruption contributes to chronic obstructive pulmonary disease (COPD). Inhibiting Hh signaling ameliorated cigarette-induced emphysema and airway inflammation in mice, suggesting a therapeutic target for smoking-related COPD.

Keywords:
chronic obstructive pulmonary disease developmentcigarette smokeemphysemahedgehog signalinginflammatory mediators

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Area of Science:

  • Pulmonary Medicine
  • Molecular Biology
  • Pathology

Background:

  • Hedgehog (Hh) signaling is crucial for embryonic development and lung quiescence.
  • Disrupted Hh signaling is implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD).
  • The role of Hh pathway in cigarette smoke-induced lung injury remains unclear.

Purpose of the Study:

  • To investigate the involvement of the Hedgehog (Hh) signaling pathway in cigarette smoke-induced emphysema and airway inflammation.
  • To determine if Hh pathway modulation affects inflammatory cytokine expression in a mouse model of COPD.
  • To explore the therapeutic potential of inhibiting Hh signaling in smoking-related lung diseases.

Main Methods:

  • C57BL/6J mice were exposed to cigarette smoke (CS) and treated with or without cyclopamine, a Hh pathway inhibitor.
  • Lung tissues were analyzed via histopathology for emphysema.
  • Gene and protein expression of sonic hedgehog (SHH), Gli1, HIP, and inflammatory mediators (ICAM-1, IL-6, IL-8, TNF-α) were quantified using RT-qPCR and Western blotting.

Main Results:

  • Cigarette smoke exposure led to emphysema and increased expression of SHH, Gli1, and inflammatory mediators.
  • Cyclopamine treatment partially ameliorated emphysema and significantly reduced SHH, Gli1, and inflammatory mediator levels.
  • Hedgehog-interacting protein (HIP) expression decreased with CS exposure but increased upon cyclopamine treatment.

Conclusions:

  • Hedgehog (Hh) signaling plays a significant role in cigarette-induced emphysema and airway inflammation by regulating inflammatory cytokines.
  • Inhibiting Hh pathway activation demonstrates therapeutic potential for smoking-related COPD.
  • Targeting the Hh signal offers a novel therapeutic strategy for COPD patients.