Title:Alterations in mRNA Expression Levels of Tight Junction Proteins in the
Blood Cells of Smokers with or without COPD
Volume: 23
Issue: 3
Author(s): Sadiya Bi Shaikh, Mahesh Manjunath Gouda, Irfan Khandhal, Tanyeem Rahman, Ashwini Shetty and Yashodhar Prabhakar Bhandary*
Affiliation:
- Yenepoya Research Centre, Yenepoya (Deemed to be University), Deralakatte, Mangalore -575018, Karnataka, India
Keywords:
Chronic obstructive pulmonary disease (COPD), Tight junction proteins (TJPs), claudins, cigarette smoke, mRNA expressions, PCR method.
Abstract:
Aim: This study aimed to assess the role of Tight junction proteins (TJPs) and claudins
in smokers with and without COPD compared to healthy individuals.
Background: Chronic obstructive pulmonary disease (COPD) is a complex chronic respiratory
disease, including various inflammatory mediators. The prime etiological element in the development
of COPD is cigarette smoking. The lung airway epithelium comprises beneficial immunological
barriers to draw in insults, such as environmental particulates, cigarette smoke, etc.
Tight junctions (TJ) connected by transmembrane proteins determine epithelial permeability.
Cigarette smoke is indicated to defect TJ integrity. The possible involvement of the airway epithelium
in the pathogenesis of COPD has recently become apparent; however, its detailed mechanisms
remain elusive. The integrity of airway epithelium is crucial for airway homeostasis; defective
airway barrier activity contributes to COPD.
Objective: In the present study, the objective was to investigate mRNA expression levels of TJP’s
like TJP-1, TJP-2, TJP-3, Tight junction-associated proteins-1, claudin-1, claudin-3, claudin-4,
claudin-7, claudin-10, claudin-15, claudin-19, and claudin-25 from blood samples of smokers
with COPD and compared them with smokers without COPD and healthy individuals.
Methods: The mRNA expressions were evaluated by the quantitative PCR method.
Results: The gene expressions of these TJPs were significantly down-regulated, specifically in
COPD patients with a history of smoking (Smokers with COPD). Besides, FEV% was also established
for these patients. Similarly, smokers with COPD showed a significant increase in the
expression levels of transcription factors, like ZEB-1, ZEB-2, PDGFA, and HDGF, compared to
COPD patients without a history of smoking (smokers without COPD) and the healthy subjects.
Conclusion: In conclusion, cigarette smoke disrupts TJ of the human airway epithelium, and the
transcriptional factors counteract this smoke-induced COPD. Thus, TJPs may serve as protective
elements for airway epithelial homeostasis during COPD.
