TY - JOUR
T1 - Pericyte-specific vascular expression of SARS-CoV-2 receptor ACE2 – implications for microvascular inflammation and hypercoagulopathy in COVID-19
AU - He, Liqun
AU - Mäe, Maarja Andaloussi
AU - Muhl, Lars
AU - Sun, Ying
AU - Pietilä, Riikka
AU - Nahar, Khayrun
AU - Vázquez Liébanas, Elisa
AU - Jonsson Fagerlund, Malin
AU - Oldner, Anders
AU - Liu, Jianping
AU - Genové, Guillem
AU - Zhang, Lei
AU - Xie, Yuan
AU - Leptidis, Stefanos
AU - Mocci, Giuseppe
AU - Stritt, Simon
AU - Osman, Ahmed M.
AU - Anisimov, Andrey
AU - Amudhala Hemanthakumar, Karthik
AU - Räsänen, Markus
AU - Mirabeau, Olivier
AU - Hansson, Emil M.
AU - Bjorkegren, Johan L. M.
AU - Vanlandewijck, Michael
AU - Blomgren, Klas
AU - Mäkinen, Taija
AU - Peng, Xiao-Rong
AU - Arnold, Thomas D.
AU - Alitalo, Kari
AU - Eriksson, Lars I
AU - Lendahl, Urban
AU - Betsholtz, Christer
PY - 2020/7/26
Y1 - 2020/7/26
N2 - Accumulating clinical observations implicatevascular inflammation as an underlyingcause of coagulopathyin severely ill COVID-19 patientsand it was recently suggested that SARS-CoV-2 virus particles infect endothelial cells.Here, we show thatendothelial cells do not expressangiotensin-converting enzyme-2 (ACE2), the SARS-CoV-2 receptor. Instead, pericytes and microvascular smooth muscle cells express ACE2 in an organotypic manner.Pericyte deficiency leads toincreased endothelial expression and releaseof Von Willebrand factorand intravascular platelet and fibrin aggregation,suggesting thatpericyteslimit endothelial pro-thromboticresponses. That pericytes and not endothelial cells express ACE2 may provide important clues tothe pathologyofCOVID-19, as pericytes are normally shielded behind anendothelial barrier and may get infected only whenthis barrier is compromisedby COVID-19 risk factors.
AB - Accumulating clinical observations implicatevascular inflammation as an underlyingcause of coagulopathyin severely ill COVID-19 patientsand it was recently suggested that SARS-CoV-2 virus particles infect endothelial cells.Here, we show thatendothelial cells do not expressangiotensin-converting enzyme-2 (ACE2), the SARS-CoV-2 receptor. Instead, pericytes and microvascular smooth muscle cells express ACE2 in an organotypic manner.Pericyte deficiency leads toincreased endothelial expression and releaseof Von Willebrand factorand intravascular platelet and fibrin aggregation,suggesting thatpericyteslimit endothelial pro-thromboticresponses. That pericytes and not endothelial cells express ACE2 may provide important clues tothe pathologyofCOVID-19, as pericytes are normally shielded behind anendothelial barrier and may get infected only whenthis barrier is compromisedby COVID-19 risk factors.
KW - 3111 Biomedicine
KW - covid-19
U2 - 10.1101/2020.05.11.088500
DO - 10.1101/2020.05.11.088500
M3 - Article
JO - bioRxiv : the preprint server for biology
JF - bioRxiv : the preprint server for biology
ER -