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SARS-CoV-2 proteins regulate inflammatory, thrombotic and diabetic responses in human arterial fibroblasts

Christopher Thor Freda1, Wei Yin1, Berhane Ghebrehiwet2

  • 1Department of Biomedical Engineering, Stony Brook University, Stony Brook, NY 11794, United States of America.

Clinical Immunology (Orlando, Fla.)
|April 25, 2021
PubMed

Insights

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) proteins trigger inflammation and thrombosis in human arterial fibroblasts. This study reveals how viral proteins impact vascular disease markers, offering insights into COVID-19 complications.

Area of Science:

  • Vascular Biology
  • Immunology
  • Virology

Background:

  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is linked to vascular complications, including thrombosis and inflammation.
  • Limited research exists on cellular responses to SARS-CoV-2 structural proteins in vascular cells.
  • Understanding these interactions is crucial for elucidating COVID-19's impact on vascular health.

Purpose of the Study:

  • To investigate the effects of SARS-CoV-2 structural proteins (Spike, Nucleocapsid, Membrane-Envelope) on human arterial adventitial fibroblasts.
  • To determine alterations in inflammatory, thrombotic, and diabetic disease markers following exposure to these viral proteins.
  • To hypothesize a mechanism for SARS-CoV-2-induced vascular disease progression.

Main Methods:

  • Human arterial adventitial fibroblasts were exposed to purified SARS-CoV-2 structural proteins.
  • Expression levels of specific proteins (gC1qR, ICAM-1, tissue factor, RAGE, GLUT-4) were measured.
  • Quantitative analysis was performed to assess up-regulation of target markers.

Main Results:

  • Exposure to SARS-CoV-2 proteins significantly up-regulated the expression of gC1qR, ICAM-1, tissue factor, RAGE, and GLUT-4 in adventitial fibroblasts.
  • The extent of protein expression varied depending on the specific SARS-CoV-2 protein involved.
  • These findings suggest distinct interaction mechanisms between different viral proteins and vascular cells.

Conclusions:

  • SARS-CoV-2 structural proteins can induce inflammatory and thrombotic responses in vascular cells.
  • The observed up-regulation of diabetic markers suggests a link between SARS-CoV-2 infection and metabolic dysregulation in the vasculature.
  • These cellular responses mediated by SARS-CoV-2 proteins may contribute to the altered vascular disease progression seen in COVID-19 patients.
Keywords:
COVID-19CardiovascularComplementInflammationSARS-CoV-2Thrombosis

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