Increased expression of CD38 on endothelial cells in SARS-CoV-2 infection in cynomolgus macaques
Copyright © 2024 Elsevier Inc. All rights reserved..
SARS-CoV-2 infection causes activation of endothelial cells (ECs), leading to dysmorphology and dysfunction. To study the pathogenesis of endotheliopathy, the activation of ECs in lungs of cynomolgus macaques after SARS-CoV-2 infection and changes in nicotinamide adenine dinucleotide (NAD) metabolism in ECs were investigated, with a focus on the CD38 molecule, which degrades NAD in inflammatory responses after SARS-CoV-2 infection. Activation of ECs was seen from day 3 after SARS-CoV-2 infection in macaques, with increases of intravascular fibrin and NAD metabolism-associated enzymes including CD38. In vitro, upregulation of CD38 mRNA in human ECs was detected after interleukin 6 (IL-6) trans-signaling induction, which was increased in the infection. In the presence of IL-6 trans-signaling stimulation, however, CD38 mRNA silencing induced significant IL-6 mRNA upregulation in ECs and promoted EC apoptosis after stimulation. These results suggest that upregulation of CD38 in patients with COVID-19 has a protective role against IL-6 trans-signaling stimulation induced by SARS-CoV-2 infection.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2024 |
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| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:594 |
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| Enthalten in: |
Virology - 594(2024) vom: 20. Apr., Seite 110052 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Nguyen, Cong Thanh [VerfasserIn] |
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| Links: |
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| Themen: |
0U46U6E8UK |
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| Anmerkungen: |
Date Completed 09.04.2024 Date Revised 09.04.2024 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1016/j.virol.2024.110052 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| 520 | |a SARS-CoV-2 infection causes activation of endothelial cells (ECs), leading to dysmorphology and dysfunction. To study the pathogenesis of endotheliopathy, the activation of ECs in lungs of cynomolgus macaques after SARS-CoV-2 infection and changes in nicotinamide adenine dinucleotide (NAD) metabolism in ECs were investigated, with a focus on the CD38 molecule, which degrades NAD in inflammatory responses after SARS-CoV-2 infection. Activation of ECs was seen from day 3 after SARS-CoV-2 infection in macaques, with increases of intravascular fibrin and NAD metabolism-associated enzymes including CD38. In vitro, upregulation of CD38 mRNA in human ECs was detected after interleukin 6 (IL-6) trans-signaling induction, which was increased in the infection. In the presence of IL-6 trans-signaling stimulation, however, CD38 mRNA silencing induced significant IL-6 mRNA upregulation in ECs and promoted EC apoptosis after stimulation. These results suggest that upregulation of CD38 in patients with COVID-19 has a protective role against IL-6 trans-signaling stimulation induced by SARS-CoV-2 infection | ||
| 650 | 4 | |a Journal Article | |
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| 650 | 4 | |a Cynomolgus macaques | |
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| 650 | 4 | |a Interleukin-6 trans-signaling | |
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| 700 | 1 | |a Kitagawa, Yoshinori |e verfasserin |4 aut | |
| 700 | 1 | |a Kakino, Akemi |e verfasserin |4 aut | |
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| 700 | 1 | |a Suzuki, Yasuhiko |e verfasserin |4 aut | |
| 700 | 1 | |a Sawamura, Tatsuya |e verfasserin |4 aut | |
| 700 | 1 | |a Kida, Hiroshi |e verfasserin |4 aut | |
| 700 | 1 | |a Itoh, Yasushi |e verfasserin |4 aut | |
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