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Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 ERJ+Open+Res 2020 ; 6 (4): ä Nephropedia Template TP
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Alteration in angiotensin-converting enzyme 2 by PM(1) during the development of emphysema in rats #MMPMID33043050
Chuang HC; Chen YY; Hsiao TC; Chou HC; Kuo HP; Feng PH; Ho SC; Chen JK; Chuang KJ; Lee KY
ERJ Open Res 2020[Oct]; 6 (4): ä PMID33043050show ga
INTRODUCTION: Angiotensin-converting enzyme 2 (ACE2) provides an adhesion site for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Patients with COPD could have severe outcomes after SARS-CoV-2 infection. The objective of this study was to investigate ACE2 regulation by air pollution during the development of COPD. METHODS: Sprague Dawley rats were exposed to unconcentrated traffic-related air pollution for 3 and 6 months. We examined lung injury markers, oxidative stress, inflammation, emphysema, ACE2 and angiotensin II receptor type 1 (AT1) and 2 (AT2) in the lungs after exposure. RESULTS: Lung injury occurred due to an increase in permeability and lactate dehydrogenase cytotoxicity was observed after 6 months of exposure to fine particulate matter of <1 mum in aerodynamic diameter (PM(1)). An alpha(1)-antitrypsin deficiency and neutrophil elastase production with emphysema development were observed after 6 months of PM(1) exposure. 8-isoprostane and interleukin-6 were increased after 3 and 6 months of PM(1) exposure. Caspase-3 was increased after exposure to PM(1) for 6 months. Upregulation of ACE2 was found after 3 months of PM(1) exposure; however, ACE2 had decreased by 6 months of PM(1) exposure. AT1 and AT2 had significantly decreased after exposure to PM(1) for 6 months. Furthermore, smooth muscle hypertrophy had occurred after 6 months of PM(1) exposure. CONCLUSIONS: In conclusion, short-term exposure to PM(1) increased the ACE2 overexpression in lungs. Long-term exposure to PM(1) decreased the ACE2 overexpression in emphysema. Air pollution may be a risk for SARS-CoV-2 adhesion during the development of COPD.