CD147 Promoted Epithelial Mesenchymal Transition in Airway Epithelial Cells Induced by Cigarette Smoke via Oxidative Stress Signaling Pathway

COPD. 2020 Jun;17(3):269-279. doi: 10.1080/15412555.2020.1758051. Epub 2020 May 5.

Abstract

Chronic obstructive pulmonary disease (COPD) is a common airway disease, and epithelial mesenchymal transition (EMT) is participated in the pathogenesis of COPD. However, the role of CD147 in COPD remains largely unknown. In order to clarify the role of CD147 in EMT induced by cigarette smoke, we established animal and cell model of EMT by mean of cigarette smoke exposure and detected the expressions of CD147 and EMT markers via PCR, WB and IF. RNA inference was applied to study the role of CD147 in CSE induced EMT in vitro. NAC and H2O2 were used to study oxidative stress signaling pathway in this model. As a result, cigarette smoke exposure upregulated the expressions of CD147, α-SMA, and Vimentin and downregulated the expression of Ecadherin and ZO1 both in vivo and in vitro, which was accompanied by augmented level of oxidative stress. CD147 knockdown would partly inhibit CSE induced EMT, while preincubation of H2O2 could inverse this effect. In conclusion, CD147 promoted EMT in mice and HBE cells induced by cigarette smoke via oxidative stress signaling pathway.

Keywords: CD147; Chronic obstructive pulmonary disease (COPD); HBE; cigarette smoke; epithelial mesenchymal transition (EMT).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / genetics
  • Animals
  • Basigin / genetics*
  • Cadherins / genetics
  • Cell Line
  • Cigarette Smoking / genetics*
  • Cigarette Smoking / metabolism
  • Cigarette Smoking / pathology
  • Epithelial Cells / metabolism*
  • Epithelial Cells / pathology
  • Epithelial-Mesenchymal Transition / genetics*
  • Gene Knockdown Techniques
  • Humans
  • In Vitro Techniques
  • Mice
  • Oxidative Stress / genetics*
  • Pulmonary Disease, Chronic Obstructive / genetics*
  • Pulmonary Disease, Chronic Obstructive / metabolism
  • Pulmonary Disease, Chronic Obstructive / pathology
  • RNA Interference
  • Real-Time Polymerase Chain Reaction
  • Respiratory Mucosa / cytology
  • Respiratory Mucosa / metabolism
  • Respiratory Mucosa / pathology
  • Signal Transduction
  • Smoke*
  • Tobacco Products*
  • Vimentin / genetics
  • Zonula Occludens-1 Protein / genetics

Substances

  • ACTA2 protein, human
  • Actins
  • Cadherins
  • Smoke
  • Vimentin
  • Zonula Occludens-1 Protein
  • alpha-smooth muscle actin, mouse
  • Basigin