Cardiomyocytes recruit monocytes upon SARS-CoV-2 infection by secreting CCL2.
Animals
COVID-19
/ pathology
Cell Communication
/ physiology
Cell Line
Chemokine CCL2
/ metabolism
Chlorocebus aethiops
Cricetinae
Disease Models, Animal
Heart Injuries
/ virology
Humans
Macrophages
/ immunology
Male
Monocytes
/ immunology
Myocytes, Cardiac
/ metabolism
Pluripotent Stem Cells
/ cytology
Vero Cells
CCL2
COVID-19
cardiomyocyte
hPSC
hamster
immune cell infiltration
Journal
Stem cell reports
ISSN: 2213-6711
Titre abrégé: Stem Cell Reports
Pays: United States
ID NLM: 101611300
Informations de publication
Date de publication:
14 09 2021
14 09 2021
Historique:
received:
06
07
2021
revised:
15
07
2021
accepted:
16
07
2021
pubmed:
18
8
2021
medline:
30
9
2021
entrez:
17
8
2021
Statut:
ppublish
Résumé
Heart injury has been reported in up to 20% of COVID-19 patients, yet the cause of myocardial histopathology remains unknown. Here, using an established in vivo hamster model, we demonstrate that SARS-CoV-2 can be detected in cardiomyocytes of infected animals. Furthermore, we found damaged cardiomyocytes in hamsters and COVID-19 autopsy samples. To explore the mechanism, we show that both human pluripotent stem cell-derived cardiomyocytes (hPSC-derived CMs) and adult cardiomyocytes (CMs) can be productively infected by SARS-CoV-2, leading to secretion of the monocyte chemoattractant cytokine CCL2 and subsequent monocyte recruitment. Increased CCL2 expression and monocyte infiltration was also observed in the hearts of infected hamsters. Although infected CMs suffer damage, we find that the presence of macrophages significantly reduces SARS-CoV-2-infected CMs. Overall, our study provides direct evidence that SARS-CoV-2 infects CMs in vivo and suggests a mechanism of immune cell infiltration and histopathology in heart tissues of COVID-19 patients.
Identifiants
pubmed: 34403650
pii: S2213-6711(21)00378-7
doi: 10.1016/j.stemcr.2021.07.012
pmc: PMC8289700
pii:
doi:
Substances chimiques
CCL2 protein, human
0
Chemokine CCL2
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
2274-2288Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK130454
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK119667
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK124463
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK127777
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK116075
Pays : United States
Organisme : American Heart Association-American Stroke Association
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK121072
Pays : United States
Commentaires et corrections
Type : UpdateOf
Type : ErratumIn
Informations de copyright
Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.
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