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Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Nat+Commun 2020 ; 11 (1): 5453 Nephropedia Template TP
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ACE2 localizes to the respiratory cilia and is not increased by ACE inhibitors or ARBs #MMPMID33116139
Lee IT; Nakayama T; Wu CT; Goltsev Y; Jiang S; Gall PA; Liao CK; Shih LC; Schurch CM; McIlwain DR; Chu P; Borchard NA; Zarabanda D; Dholakia SS; Yang A; Kim D; Chen H; Kanie T; Lin CD; Tsai MH; Phillips KM; Kim R; Overdevest JB; Tyler MA; Yan CH; Lin CF; Lin YT; Bau DT; Tsay GJ; Patel ZM; Tsou YA; Tzankov A; Matter MS; Tai CJ; Yeh TH; Hwang PH; Nolan GP; Nayak JV; Jackson PK
Nat Commun 2020[Oct]; 11 (1): 5453 PMID33116139show ga
The coronavirus SARS-CoV-2 is the causative agent of the ongoing severe acute respiratory disease pandemic COVID-19. Tissue and cellular tropism is one key to understanding the pathogenesis of SARS-CoV-2. We investigate the expression and subcellular localization of the SARS-CoV-2 receptor, angiotensin-converting enzyme 2 (ACE2), within the upper (nasal) and lower (pulmonary) respiratory tracts of human donors using a diverse panel of banked tissues. Here, we report our discovery that the ACE2 receptor protein robustly localizes within the motile cilia of airway epithelial cells, which likely represents the initial or early subcellular site of SARS-CoV-2 viral entry during host respiratory transmission. We further determine whether ciliary ACE2 expression in the upper airway is influenced by patient demographics, clinical characteristics, comorbidities, or medication use, and show the first mechanistic evidence that the use of angiotensin-converting enzyme inhibitors (ACEI) or angiotensin II receptor blockers (ARBs) does not increase susceptibility to SARS-CoV-2 infection through enhancing the expression of ciliary ACE2 receptor. These findings are crucial to our understanding of the transmission of SARS-CoV-2 for prevention and control of this virulent pathogen.