Sayantan Datta1, Hae-Seong Nam2, Masamichi Hayashi1, Leonel Maldonado1, Rachel Goldberg1, Mariana Brait1, David Sidransky1, Peter Illei3, Alex Baras3, Neeraj Vij4, Mohammad O Hoque5. 1. Department of Otolaryngology and Head & Neck Surgery, The Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA. 2. Department of Otolaryngology and Head & Neck Surgery, The Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA; Division of Pulmonology, Department of Internal Medicine, Inha University Hospital, Inha University School of Medicine, Incheon, 22332, South Korea. 3. Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA. 4. College of Medicine, Central Michigan University, Mount Pleasant, MI, 48859, USA; Department of Pediatric Respiratory Sciences, The Johns Hopkins University School of Medicine, Baltimore, MD, 21236, USA. 5. Department of Otolaryngology and Head & Neck Surgery, The Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA; Department of Oncology, The Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA; Department of Urology, The Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA. Electronic address: mhoque1@jhmi.edu.
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, χ2 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.
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 COPDpatients, however, GULP1 expression was detected at different levels in bronchial epithelium. GULP1 expression statistically correlated with severity of COPD-emphysema (p = 0.001, χ2 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.
Authors: Stephen D Larcombe; Paul Capewell; Kirsty Jensen; William Weir; Jane Kinnaird; Elizabeth J Glass; Brian R Shiels Journal: PLoS One Date: 2022-01-21 Impact factor: 3.240