Human pulmonary artery endothelial cells upregulate ACE2 expression in response to iron-regulatory elements: Potential implications for SARS-CoV-2 infection.

Abstract

Vascular endothelial cell dysfunction is reported in severe coronavirus disease 2019 disease, however, controversy exists regarding levels of angiotensin‐converting enzyme 2 (ACE2) expression, a coreceptor for severe acute respiratory syndrome coronavirus 2, in these cells. We report ACE2 expression and positive regulation by both interleuki‐6, hepcidin, and ferroportin knock‐down in pulmonary artery endothelial cells with potential implications for viral infection.