Changes in Adenosine Deaminase Activity and Endothelial Dysfunction after Mild Coronavirus Disease-2019

Author:

Jedrzejewska Agata1ORCID,Kawecka Ada1ORCID,Braczko Alicja1ORCID,Romanowska-Kocejko Marzena2,Stawarska Klaudia1ORCID,Deptuła Milena3ORCID,Zawrzykraj Małgorzata4ORCID,Franczak Marika1ORCID,Krol Oliwia1ORCID,Harasim Gabriela1ORCID,Walczak Iga1,Pikuła Michał3ORCID,Hellmann Marcin2,Kutryb-Zając Barbara1ORCID

Affiliation:

1. Department of Biochemistry, Medical University of Gdansk, 80-211 Gdansk, Poland

2. Department of Cardiac Diagnostics, Medical University of Gdansk, 80-210 Gdansk, Poland

3. Laboratory of Tissue Engineering and Regenerative Medicine, Division of Embryology, Medical University of Gdansk, 80-211 Gdansk, Poland

4. Division of Clinical Anatomy, Department of Anatomy, Medical University of Gdansk, 80-210 Gdansk, Poland

Abstract

Endothelial cells are a preferential target for SARS-CoV-2 infection. Previously, we have reported that vascular adenosine deaminase 1 (ADA1) may serve as a biomarker of endothelial activation and vascular inflammation, while ADA2 plays a critical role in monocyte and macrophage function. In this study, we investigated the activities of circulating ADA isoenzymes in patients 8 weeks after mild COVID-19 and related them to the parameters of inflammation and microvascular/endothelial function. Post-COVID patients revealed microvascular dysfunction associated with the changes in circulating parameters of endothelial dysfunction and inflammatory activation. Interestingly, serum total ADA and ADA2 activities were diminished in post-COVID patients, while ADA1 remained unchanged in comparison to healthy controls without a prior diagnosis of SARS-CoV-2 infection. While serum ADA1 activity tended to positively correspond with the parameters of endothelial activation and inflammation, sICAM-1 and TNFα, serum ADA2 activity correlated with IL-10. Simultaneously, post-COVID patients had lower circulating levels of ADA1-anchoring protein, CD26, that may serve as an alternative receptor for virus binding. This suggests that after the infection CD26 is rather maintained in cell-attached form, enabling ADA1 complexing. This study points to the possible role of ADA isoenzymes in cardiovascular complications after mild COVID-19.

Funder

National Science Centre of Poland

Publisher

MDPI AG

Subject

Inorganic Chemistry,Organic Chemistry,Physical and Theoretical Chemistry,Computer Science Applications,Spectroscopy,Molecular Biology,General Medicine,Catalysis

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