SnRNA sequencing defines signaling by RBC-derived extracellular vesicles in the murine heart.
Animals
Cell Communication
/ genetics
Cell Proliferation
/ genetics
Cells, Cultured
Disease Models, Animal
Erythrocytes
/ metabolism
Extracellular Vesicles
/ metabolism
Female
Healthy Volunteers
Heart Failure
/ blood
Humans
Male
Mice
Mice, Inbred C57BL
Mice, Transgenic
Myocardial Infarction
/ blood
Myocardium
/ metabolism
Myocytes, Cardiac
/ metabolism
RNA, Nuclear
/ genetics
RNA-Seq
/ methods
Signal Transduction
/ genetics
Single-Cell Analysis
/ methods
Journal
Life science alliance
ISSN: 2575-1077
Titre abrégé: Life Sci Alliance
Pays: United States
ID NLM: 101728869
Informations de publication
Date de publication:
12 2021
12 2021
Historique:
received:
05
02
2021
revised:
30
09
2021
accepted:
30
09
2021
entrez:
19
10
2021
pubmed:
20
10
2021
medline:
23
3
2022
Statut:
epublish
Résumé
Extracellular vesicles (EVs) mediate intercellular signaling by transferring their cargo to recipient cells, but the functional consequences of signaling are not fully appreciated. RBC-derived EVs are abundant in circulation and have been implicated in regulating immune responses. Here, we use a transgenic mouse model for fluorescence-based mapping of RBC-EV recipient cells to assess the role of this intercellular signaling mechanism in heart disease. Using fluorescent-based mapping, we detected an increase in RBC-EV-targeted cardiomyocytes in a murine model of ischemic heart failure. Single cell nuclear RNA sequencing of the heart revealed a complex landscape of cardiac cells targeted by RBC-EVs, with enrichment of genes implicated in cell proliferation and stress signaling pathways compared with non-targeted cells. Correspondingly, cardiomyocytes targeted by RBC-EVs more frequently express cellular markers of DNA synthesis, suggesting the functional significance of EV-mediated signaling. In conclusion, our mouse model for mapping of EV-recipient cells reveals a complex cellular network of RBC-EV-mediated intercellular communication in ischemic heart failure and suggests a functional role for this mode of intercellular signaling.
Identifiants
pubmed: 34663679
pii: 4/12/e202101048
doi: 10.26508/lsa.202101048
pmc: PMC8548207
pii:
doi:
Substances chimiques
RNA, Nuclear
0
Banques de données
Dryad
['10.5061/dryad.vhhmgqnv9']
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NHLBI NIH HHS
ID : R35 HL150807
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL150401
Pays : United States
Organisme : NCATS NIH HHS
ID : UH3 TR002881
Pays : United States
Organisme : NCATS NIH HHS
ID : UG3 TR002881
Pays : United States
Organisme : NCATS NIH HHS
ID : UH3 TR002878
Pays : United States
Organisme : NICHD NIH HHS
ID : T32 HD007203
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA218500
Pays : United States
Organisme : NCATS NIH HHS
ID : UG3 TR002878
Pays : United States
Organisme : NHLBI NIH HHS
ID : UG3 HL147353
Pays : United States
Informations de copyright
© 2021 Valkov et al.
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