Alterations in mRNA Expression Levels of Tight Junction Proteins in the Blood Cells of Smokers with or without COPD

TY - JOUR

T1 - Alterations in mRNA Expression Levels of Tight Junction Proteins in the Blood Cells of Smokers with or without COPD

AU - Shaikh, Sadiya Bi

AU - Gouda, Mahesh Manjunath

AU - K, Irfan

AU - Rahman, Tanyeem

AU - Shetty, Ashwini

AU - Bhandary, Yashodhar Prabhakar

N1 - Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.

PY - 2023

Y1 - 2023

N2 - 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.

AB - 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.

U2 - 10.2174/1871530322666220531121609

DO - 10.2174/1871530322666220531121609

M3 - SCORING: Journal article

C2 - 35642119

VL - 23

SP - 389

EP - 395

JO - ENDOCR METAB IMMUNE

JF - ENDOCR METAB IMMUNE

SN - 1871-5303

IS - 3

ER -