title: Vitronectin expression in the airways of subjects with asthma and chronic obstructive pulmonary disease.
abstract: Vitronectin, a multifunctional glycoprotein, is involved in coagulation, inhibition of the formation of the membrane attack complex (MAC), cell adhesion and migration, wound healing, and tissue remodeling. The primary cellular source of vitronectin is hepatocytes; it is not known whether resident cells of airways produce vitronectin, even though the glycoprotein has been found in exhaled breath condensate and bronchoalveolar lavage from healthy subjects and patients with interstitial lung disease. It is also not known whether vitronectin expression is altered in subjects with asthma and COPD. In this study, bronchial tissue from 7 asthmatic, 10 COPD and 14 control subjects was obtained at autopsy and analyzed by immunohistochemistry to determine the percent area of submucosal glands occupied by vitronectin. In a separate set of experiments, quantitative colocalization analysis was performed on tracheobronchial tissue sections obtained from donor lungs (6 asthmatics, 4 COPD and 7 controls). Vitronectin RNA and protein expressions in bronchial surface epithelium were examined in 12 subjects who undertook diagnostic bronchoscopy. Vitronectin was found in the tracheobronchial epithelium from asthmatic, COPD, and control subjects, although its expression was significantly lower in the asthmatic group. Colocalization analysis of 3D confocal images indicates that vitronectin is expressed in the glandular serous epithelial cells and in respiratory surface epithelial cells other than goblet cells. Expression of the 65-kDa vitronectin isoform was lower in bronchial surface epithelium from the diseased subjects. The cause for the decreased vitronectin expression in asthma is not clear, however, the reduced concentration of vitronectin in the epithelial/submucosal layer of airways may be linked to airway remodeling.
authors.affiliation: School of Medicine, Universidad CES, Medellín, Colombia.
authors.forename: Lina M
authors.initials: LM
authors.lastname: Salazar-Peláez
authors.affiliation: Penn State Microscopy Imaging Core, Penn State Hershey College of Medicine, Hershey, Pennsylvania, United States of America.
authors.forename: Thomas
authors.initials: T
authors.lastname: Abraham
authors.affiliation: School of Medicine, Universidad CES, Medellín, Colombia.
authors.forename: Ana M
authors.initials: AM
authors.lastname: Herrera
authors.affiliation: Instituto Nacional de Medicina Legal y Ciencias Forenses, Medellín, Colombia.
authors.forename: Mario A
authors.initials: MA
authors.lastname: Correa
authors.affiliation: Clínica Cardio VID, Medellín, Colombia.
authors.forename: Jorge E
authors.initials: JE
authors.lastname: Ortega
authors.affiliation: James Hogg Research Centre, University of British Columbia, Vancouver, BC, Canada.
authors.forename: Peter D
authors.initials: PD
authors.lastname: Paré
authors.affiliation: School of Medicine, Universidad CES, Medellín, Colombia; James Hogg Research Centre, University of British Columbia, Vancouver, BC, Canada.
authors.forename: Chun Y
authors.initials: CY
authors.lastname: Seow
mesh_terms: D000328:Adult; D000368:Aged; D001249:Asthma / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D001980:Bronchi / Q000378:metabolism* / Q000473:pathology; D016022:Case-Control Studies; D004847:Epithelial Cells / Q000378:metabolism; D005088:Exocrine Glands / Q000473:pathology; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D008297:Male; D008875:Middle Aged; D020033:Protein Isoforms / Q000235:genetics / Q000378:metabolism; D029424:Pulmonary Disease, Chronic Obstructive / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D019096:Vitronectin / Q000235:genetics / Q000378:metabolism*; D055815:Young Adult
chemical_list: D020033:Protein Isoforms; D019096:Vitronectin