TY - JOUR
T1 - Changes in Adenosine Deaminase Activity and Endothelial Dysfunction after Mild Coronavirus Disease-2019
AU - Jedrzejewska, Agata
AU - Kawecka, Ada
AU - Braczko, Alicja
AU - Romanowska-Kocejko, Marzena
AU - Stawarska, Klaudia
AU - Deptuła, Milena
AU - Zawrzykraj, Małgorzata
AU - Franczak, Marika
AU - Krol, Oliwia
AU - Harasim, Gabriela
AU - Walczak, Iga
AU - Pikuła, Michał
AU - Hellmann, Marcin
AU - Kutryb-Zając, Barbara
N1 - Funding Information: This research was supported by the National Science Centre of Poland, grant number 2019/35/D/NZ3/03512. Publisher Copyright: © 2023 by the authors.
PY - 2023/9/1
Y1 - 2023/9/1
N2 - 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.
AB - 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.
KW - COVID-19
KW - adenosine deaminase
KW - endothelium
KW - microvascular dysfunction
UR - http://www.scopus.com/inward/record.url?scp=85170226864&partnerID=8YFLogxK
U2 - https://doi.org/10.3390/ijms241713140
DO - https://doi.org/10.3390/ijms241713140
M3 - Article
C2 - 37685949
SN - 1661-6596
VL - 24
JO - International journal of molecular sciences
JF - International journal of molecular sciences
IS - 17
M1 - 13140
ER -