tetano
Editor, Senior Moderator
Clin Immunol
. 2021 Apr 22;108733.
doi: 10.1016/j.clim.2021.108733. Online ahead of print.
SARS-CoV-2 proteins regulate inflammatory, thrombotic and diabetic responses in human arterial fibroblasts
Christopher Thor Freda[SUP] 1 [/SUP], Wei Yin[SUP] 1 [/SUP], Berhane Ghebrehiwet[SUP] 2 [/SUP], David A Rubenstein[SUP] 3 [/SUP]
Affiliations
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for many pathological processes, including altered vascular disease development, dysfunctional thrombosis and a heightened inflammation. However, there is limited work to determine the underlying cellular responses induced by exposure to SARS-CoV-2 proteins. Thus, our objective was to investigate how human arterial adventitial fibroblasts inflammation, thrombosis and diabetic disease markers are altered in response to Spike, Nucleocapsid and Membrane-Envelope Proteins. We hypothesized that after a short-term exposure to SARS-CoV-2 proteins, adventitial fibroblasts would have a higher expression of inflammatory, thrombotic and diabetic proteins, which would support a mechanism for altered vascular disease progression. After incubation, the expression of gC1qR, ICAM-1, tissue factor, RAGE and GLUT-4 was significantly up-regulated. In general, the extent of expression was different for each SARS-CoV-2 proteins, suggesting that SARS-CoV-2 proteins interacts with cells through different mechanisms. Thus, SARS-CoV-2 protein interaction with vascular cells may regulate vascular disease responses.
Keywords: COVID-19; Cardiovascular; Complement; Inflammation; SARS-CoV-2; Thrombosis.
. 2021 Apr 22;108733.
doi: 10.1016/j.clim.2021.108733. Online ahead of print.
SARS-CoV-2 proteins regulate inflammatory, thrombotic and diabetic responses in human arterial fibroblasts
Christopher Thor Freda[SUP] 1 [/SUP], Wei Yin[SUP] 1 [/SUP], Berhane Ghebrehiwet[SUP] 2 [/SUP], David A Rubenstein[SUP] 3 [/SUP]
Affiliations
- PMID: 33895357
- DOI: 10.1016/j.clim.2021.108733
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for many pathological processes, including altered vascular disease development, dysfunctional thrombosis and a heightened inflammation. However, there is limited work to determine the underlying cellular responses induced by exposure to SARS-CoV-2 proteins. Thus, our objective was to investigate how human arterial adventitial fibroblasts inflammation, thrombosis and diabetic disease markers are altered in response to Spike, Nucleocapsid and Membrane-Envelope Proteins. We hypothesized that after a short-term exposure to SARS-CoV-2 proteins, adventitial fibroblasts would have a higher expression of inflammatory, thrombotic and diabetic proteins, which would support a mechanism for altered vascular disease progression. After incubation, the expression of gC1qR, ICAM-1, tissue factor, RAGE and GLUT-4 was significantly up-regulated. In general, the extent of expression was different for each SARS-CoV-2 proteins, suggesting that SARS-CoV-2 proteins interacts with cells through different mechanisms. Thus, SARS-CoV-2 protein interaction with vascular cells may regulate vascular disease responses.
Keywords: COVID-19; Cardiovascular; Complement; Inflammation; SARS-CoV-2; Thrombosis.