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1. The cytoprotective role of DJ-1 and p45 NFE2 against human primary alveolar type II cell injury and emphysema

Author

Li Hui Tan, Karim Bahmed, Chih-Ru Lin, Nathaniel Marchetti, Sudhir Bolla, Gerard J. Criner, Steven Kelsen, Muniswamy Madesh, and Beata Kosmider

Subjects
Medicine, Science
Abstract

Abstract Emphysema is characterized by irreversibly enlarged airspaces and destruction of alveolar walls. One of the factors contributing to this disease pathogenesis is an elevation in extracellular matrix (ECM) degradation in the lung. Alveolar type II (ATII) cells produce and secrete pulmonary surfactants and proliferate to restore the epithelium after damage. We isolated ATII cells from control non-smokers, smokers and patients with emphysema to determine the role of NFE2 (nuclear factor, erythroid-derived 2). NFE2 is a heterodimer composed of two subunits, a 45 kDa (p45 NFE2) and 18 kDa (p18 NFE2) polypeptides. Low expression of p45 NFE2 in patients with emphysema correlated with a high ECM degradation. Moreover, we found that NFE2 knockdown increased cell death induced by cigarette smoke extract. We also studied the cross talk between p45 NFE2 and DJ-1. DJ-1 protein is a redox-sensitive chaperone that protects cells from oxidative stress. We detected that cigarette smoke significantly increased p45 NFE2 levels in DJ-1 KO mice compared to wild-type mice. Our results indicate that p45 NFE2 expression is induced by exposure to cigarette smoke, has a cytoprotective activity against cell injury, and its downregulation in human primary ATII cells may contribute to emphysema pathogenesis.

Published
2018
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2. The cytoprotective role of DJ-1 and p45 NFE2 against human primary alveolar type II cell injury and emphysema

Author

Li Hui Tan, Sudhir Bolla, Karim Bahmed, Gerard J. Criner, Muniswamy Madesh, Chih-Ru Lin, Nathaniel Marchetti, Steven G. Kelsen, and Beata Kosmider

Subjects
0301 basic medicine, Programmed cell death, Science, Protein Deglycase DJ-1, medicine.disease_cause, Article, Cigarette Smoking, Extracellular matrix, Pathogenesis, 03 medical and health sciences, 0302 clinical medicine, Downregulation and upregulation, medicine, Animals, Humans, Secretion, Lung, Cell Proliferation, Emphysema, Mice, Knockout, Multidisciplinary, Chemistry, Cell growth, respiratory system, 3. Good health, Extracellular Matrix, Pulmonary Alveoli, 030104 developmental biology, medicine.anatomical_structure, 030228 respiratory system, Gene Expression Regulation, NF-E2 Transcription Factor, p45 Subunit, Cancer research, Medicine, Oxidative stress
Abstract

Emphysema is characterized by irreversibly enlarged airspaces and destruction of alveolar walls. One of the factors contributing to this disease pathogenesis is an elevation in extracellular matrix (ECM) degradation in the lung. Alveolar type II (ATII) cells produce and secrete pulmonary surfactants and proliferate to restore the epithelium after damage. We isolated ATII cells from control non-smokers, smokers and patients with emphysema to determine the role of NFE2 (nuclear factor, erythroid-derived 2). NFE2 is a heterodimer composed of two subunits, a 45 kDa (p45 NFE2) and 18 kDa (p18 NFE2) polypeptides. Low expression of p45 NFE2 in patients with emphysema correlated with a high ECM degradation. Moreover, we found that NFE2 knockdown increased cell death induced by cigarette smoke extract. We also studied the cross talk between p45 NFE2 and DJ-1. DJ-1 protein is a redox-sensitive chaperone that protects cells from oxidative stress. We detected that cigarette smoke significantly increased p45 NFE2 levels in DJ-1 KO mice compared to wild-type mice. Our results indicate that p45 NFE2 expression is induced by exposure to cigarette smoke, has a cytoprotective activity against cell injury, and its downregulation in human primary ATII cells may contribute to emphysema pathogenesis.

Published
2017

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