Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/135740
Title: Is the purinergic pathway involved in the pathology of COPD? Decreased lung CD39 expression at initial stages of COPD
Author: Aliagas, Elisabet
Muñoz Esquerre, Mariana
Cuevas, Ester
Careta, Oriol
Huertas, Daniel
López Sánchez, Marta
Escobar Campuzano, Ignacio
Dorca i Sargatal, Jordi
Santos Pérez, Salud
Keywords: Malalties pulmonars obstructives cròniques
Inflamació
Expressió gènica
Chronic obstructive pulmonary diseases
Inflammation
Gene expression
Issue Date: 28-May-2018
Publisher: BioMed Central
Abstract: Background: Extracellular adenosine triphosphate (ATP) is up-regulated in the airways of patients with chronic obstructive pulmonary disease (COPD), resulting in increased inflammation, bronchoconstriction, and cough. Although extracellular ATP levels are tightly controlled by nucleoside triphosphate diphosphohydrolase-1 (NTPDase1; also known as CD39) in the lungs, the role of CD39 in the pathology of COPD is unknown. We hypothesized that alterations in the expression and activity of CD39 could be part of the mechanisms for initiating and perpetuating the disease. Methods: We analyzed CD39 gene and protein expression as well as ATPase enzyme activity in lung tissue samples of patients with COPD (n = 17), non-obstructed smokers (NOS) (n = 16), and never smokers (NS) (n = 13). Morphometry studies were performed to analyze pulmonary vascular remodeling. Results: There was significantly decreased CD39 gene expression in the lungs of the COPD group (1.17 [0.85-1.81]) compared with the NOS group (1.88 [1.35-4.41]) and NS group (3.32 [1.23-5.39]) (p = 0.037). This attenuation correlated with higher systemic inflammation and intimal thickening of muscular pulmonary arteries in the COPD group. Lung CD39 protein levels were also lower in the COPD group (0.34 [0.22-0.92]) compared with the NOS group (0.67 [0.32-1.06]) and NS group (0.95 [0.4-1.1) (p = 0.133). Immunohistochemistry showed that CD39 was downregulated in lung parenchyma, epithelial bronchial cells, and the endothelial cells of pulmonary muscular arteries in the COPD group. ATPase activity in human pulmonary structures was reduced in the lungs of patients with COPD. Conclusion: An attenuation of CD39 expression and activity is presented in lung tissue of stable COPD patients, which could lead to pulmonary ATP accumulation, favoring the development of pulmonary inflammation and emphysema. This may be a mechanism underlying the development of COPD.
Note: Reproducció del document publicat a: https://doi.org/10.1186/s12931-018-0793-0
It is part of: Respiratory Research, 2018, vol. 19, num. 1, p. 103-113
URI: http://hdl.handle.net/2445/135740
Related resource: https://doi.org/10.1186/s12931-018-0793-0
ISSN: 1465-993X
Appears in Collections:Articles publicats en revistes (Ciències Clíniques)
Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL))

Files in This Item:
File Description SizeFormat 
680151.pdf5.97 MBAdobe PDFView/Open


This item is licensed under a Creative Commons License Creative Commons