Expression of GULP1 in bronchial epithelium is associated with the progression of emphysema in chronic obstructive pulmonary disease. (March 2017)

• Record Type: Journal Article
• Authors: Datta, Sayantan; Nam, Hae-Seong; Hayashi, Masamichi; Maldonado, Leonel; Goldberg, Rachel; Brait, Mariana; Sidransky, David; Illei, Peter; Baras, Alex; Vij, Neeraj; Hoque, Mohammad O.
• Is Part Of: Respiratory medicine. Volume 124(2017)
• Page Start: 72
• Page End: 78
• Publication Date: 2017-03
• Subjects: GULP1 -- Chronic obstructive pulmonary disease -- Emphysema -- Bronchial tissue -- Lung parenchyma; AM alveolar macrophage -- COPD chronic obstructive pulmonary disease -- FEV1 forced expiratory volume in 1 second -- FFPE formalin-fixed paraffin-embedded -- FVC forced vital capacity -- GOLD Global Initiative for Chronic Obstructive Lung Disease -- H & E hematoxylin & eosin -- IHC Immunohistochemistry -- NSCLC Non-small cell lung cancer -- QMSP quantitative methylation specific PCR; Chest -- Diseases -- Periodicals; Chest -- Diseases -- Great Britain -- Periodicals; Respiratory organs -- Diseases -- Periodicals; Respiratory Tract Diseases -- Periodicals; Appareil respiratoire -- Maladies -- Périodiques; Thorax -- Maladies -- Périodiques; Appareil respiratoire -- Maladies -- Traitement -- Périodiques; Electronic journals; 616.2
• DOI: 10.1016/j.rmed.2017.02.011
• Languages: English
• ISSNs: 0954-6111

Abstract

Abstract: Background: GULP1 functions as a cytoplasmic adaptor protein involved in the engulfment of apoptotic cells. The aim of this study was to investigate the expression and/or promoter methylation of GULP1 in the bronchial tissue and the lung parenchyma of chronic obstructive pulmonary disease (COPD) patients and control subjects without COPD (non-smokers and smokers). Methods: Using a case–control design, we selected a group of 15 subjects with non-small cell lung carcinoma (NSCLC), 15 subjects with COPD, 9 subjects of without COPD (4 non-smokers and 5 smokers) as controls. We studied the expression of GULP1 in the bronchial tissue and the lung parenchyma by means of immunohistochemistry (IHC). To understand the mechanistic aspect of GULP1 expression in COPD and NSCLC, we performed quantitative methylation specific PCR (QMSP) in cases and controls of COPD and NSCLC. Results: Our IHC analysis revealed that GULP1 was not expressed in pneumocytes or alveolar macrophages of COPD patients, however, GULP1 expression was detected at different levels in bronchial epithelium. GULP1 expression statistically correlated with severity of COPD-emphysema ( p = 0.001, χ 2 test). GULP1 promoter methylation was not observed by QMSP assay in any of the samples thereby excluding the role of promoter methylation in differential expression of GULP1 in COPD and NSCLC. Conclusions: This study provides preliminary observations on the differences in GULP1 expression in different cellular components of lung tissues from COPD and control subjects. Our findings suggest a potential role for GULP1 in the pathogenesis and progression of COPD-emphysema that warrants further investigation. Highlights: GULP1 functions as a cytoplasmic adaptor protein involved in the engulfment of apoptotic cells. We investigated the expression of GULP1 in lung tissues from COPD and control subjects. GULP1 expression was significantly increased in the bronchial epithelium of COPD patients with advanced GOLD stages. GULP1 may act as a novel protein in the COPD initiation and progression.