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      Angiotensin-converting enzyme 2 expression in COPD and IPF fibroblasts: the forgotten cell in COVID-19

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          The COVID-19 pandemic is associated with severe pneumonia and acute respiratory distress syndrome leading to death in susceptible individuals. For those who recover, post-COVID-19 complications may include development of pulmonary fibrosis. Factors contributing to disease severity or development of complications are not known. Using computational analysis with experimental data, we report that idiopathic pulmonary fibrosis (IPF)- and chronic obstructive pulmonary disease (COPD)-derived lung fibroblasts express higher levels of angiotensin-converting enzyme 2 (ACE2), the receptor for SARS-CoV-2 entry and part of the renin-angiotensin system that is antifibrotic and anti-inflammatory. In preclinical models, we found that chronic exposure to cigarette smoke, a risk factor for both COPD and IPF and potentially for SARS-CoV-2 infection, significantly increased pulmonary ACE2 protein expression. Further studies are needed to understand the functional implications of ACE2 on lung fibroblasts, a cell type that thus far has received relatively little attention in the context of COVID-19.

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          Most cited references 28

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          Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus–Infected Pneumonia in Wuhan, China

          In December 2019, novel coronavirus (2019-nCoV)-infected pneumonia (NCIP) occurred in Wuhan, China. The number of cases has increased rapidly but information on the clinical characteristics of affected patients is limited.
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            Is Open Access

            A pneumonia outbreak associated with a new coronavirus of probable bat origin

            Since the outbreak of severe acute respiratory syndrome (SARS) 18 years ago, a large number of SARS-related coronaviruses (SARSr-CoVs) have been discovered in their natural reservoir host, bats 1–4 . Previous studies have shown that some bat SARSr-CoVs have the potential to infect humans 5–7 . Here we report the identification and characterization of a new coronavirus (2019-nCoV), which caused an epidemic of acute respiratory syndrome in humans in Wuhan, China. The epidemic, which started on 12 December 2019, had caused 2,794 laboratory-confirmed infections including 80 deaths by 26 January 2020. Full-length genome sequences were obtained from five patients at an early stage of the outbreak. The sequences are almost identical and share 79.6% sequence identity to SARS-CoV. Furthermore, we show that 2019-nCoV is 96% identical at the whole-genome level to a bat coronavirus. Pairwise protein sequence analysis of seven conserved non-structural proteins domains show that this virus belongs to the species of SARSr-CoV. In addition, 2019-nCoV virus isolated from the bronchoalveolar lavage fluid of a critically ill patient could be neutralized by sera from several patients. Notably, we confirmed that 2019-nCoV uses the same cell entry receptor—angiotensin converting enzyme II (ACE2)—as SARS-CoV.
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              Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesis

              Abstract Severe acute respiratory syndrome (SARS) is an acute infectious disease that spreads mainly via the respiratory route. A distinct coronavirus (SARS‐CoV) has been identified as the aetiological agent of SARS. Recently, a metallopeptidase named angiotensin‐converting enzyme 2 (ACE2) has been identified as the functional receptor for SARS‐CoV. Although ACE2 mRNA is known to be present in virtually all organs, its protein expression is largely unknown. Since identifying the possible route of infection has major implications for understanding the pathogenesis and future treatment strategies for SARS, the present study investigated the localization of ACE2 protein in various human organs (oral and nasal mucosa, nasopharynx, lung, stomach, small intestine, colon, skin, lymph nodes, thymus, bone marrow, spleen, liver, kidney, and brain). The most remarkable finding was the surface expression of ACE2 protein on lung alveolar epithelial cells and enterocytes of the small intestine. Furthermore, ACE2 was present in arterial and venous endothelial cells and arterial smooth muscle cells in all organs studied. In conclusion, ACE2 is abundantly present in humans in the epithelia of the lung and small intestine, which might provide possible routes of entry for the SARS‐CoV. This epithelial expression, together with the presence of ACE2 in vascular endothelium, also provides a first step in understanding the pathogenesis of the main SARS disease manifestations. Copyright © 2004 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

                Author and article information

                Am J Physiol Lung Cell Mol Physiol
                Am J Physiol Lung Cell Mol Physiol
                Am J Physiol Lung Cell Mol Physiol
                American Journal of Physiology - Lung Cellular and Molecular Physiology
                American Physiological Society (Bethesda, MD )
                1 January 2021
                28 October 2020
                28 October 2020
                : 320
                : 1
                : L152-L157
                1Research Institute of the McGill University Health Centre , Montreal, Quebec, Canada
                2Department of Pathology, McGill University , Montreal, Quebec, Canada
                3Department of Medicine, McGill University , Montreal, Quebec, Canada
                4Department of Pharmacology and Therapeutics, McGill University , Montreal, Quebec, Canada
                5Department of Computational Biology, Carnegie Mellon University , Pittsburgh, Pennsylvania
                6Department of Medicine, McMaster University & St. Joseph’s Healthcare , Hamilton, Ontario, Canada
                7Department of Internal Medicine, University of Michigan , Ann Arbor, Michigan
                Author notes
                Correspondence: C. J. Baglole ( Carolyn.baglole@ 123456mcgill.ca ).
                L-00455-2020 L-00455-2020
                Copyright © 2021 the American Physiological Society
                Funded by: Gouvernement du Canada | CIHR | Institute of Health Services and Policy Research (IHSPR) 10.13039/501100000037
                Award Recipient : Carolyn J Baglole
                Funded by: Canada Foundation for Innovation (Fondation canadienne pour l'innovation) 10.13039/501100000196
                Award Recipient : Carolyn J Baglole
                Funded by: Fonds de Recherche du Québec-Société et Culture (FRQSC) 10.13039/100008240
                Award Recipient : Carolyn J Baglole
                Funded by: Taibah University 10.13039/501100002403
                Award Recipient : Noof Aloufi
                Rapid Report
                The Pathophysiology of COVID-19 and SARS-CoV-2 Infection
                Custom metadata

                Anatomy & Physiology

                ace2, copd, fibroblast, ipf, sars-cov-2


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