Open AccessEnhanced Bronchial Expression of Extracellular Matrix Proteins in Chronic Obstructive Pulmonary Disease
Author(s) -
Andor Kranenburg,
Anna Willems-Widyastuti,
Wolter J. Mooi,
Peter J. Sterk,
Vijay Kumar Thyagarajan Alagappan,
Willem I. de Boer,
Hari Shanker Sharma
Publication year - 2006
Publication title -
american journal of clinical pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.859
H-Index - 128
eISSN - 1943-7722
pISSN - 0002-9173
DOI - 10.1309/jc477fael1ykv54w
Subject(s) - laminin , fibronectin , extracellular matrix , copd , basement membrane , pathology , medicine , lamina propria , adventitia , immunohistochemistry , fibrosis , airway , epithelium , biology , microbiology and biotechnology , surgery
Remodeling of airways and blood vessels is an important feature in chronic obstructive pulmonary disease (COPD). By using immunohistochemical analysis, we examined bronchial expression patterns of various extracellular matrix (ECM) components such as collagens (subtypes I, III, and IV), fibronectin, and laminin beta2 in patients with COPD (forced expiratory volume in 1 second [FEV1] <or=75%; n = 15) and without COPD (FEV1 >or=85%; n = 16) and correlated expression data with lung function. Quantitative analysis revealed enhanced levels (P < .01) of total collagens I, III, and IV in surface epithelial basement membrane (SEBM) and collagens I and III in bronchial lamina propria (P < .02) and adventitia (P < .05) in COPD. Distinct and increased (P < .05) vascular expression of fibronectin accounts for intimal vascular fibrosis, whereas laminin beta2 (P < .05) was elevated in airway smooth muscle (ASM). FEV1 values inversely correlated with collagens in the SEBM, fibronectin in bronchial vessels, and laminin in the ASM. Our data suggest that COPD exhibits increased bronchial deposition of ECM proteins that contribute to deteriorated lung function and airway remodeling.