Age-related defects in autophagy alter the secretion of paracrine factors from bone marrow mononuclear cells.
Aging
/ pathology
Animals
Antigens, Ly
/ metabolism
Autophagy
/ drug effects
Autophagy-Related Protein 7
/ metabolism
Bone Marrow Cells
/ metabolism
Culture Media, Conditioned
/ pharmacology
Extracellular Vesicles
/ drug effects
Fibroblasts
/ drug effects
Leukocytes, Mononuclear
/ drug effects
Membrane Proteins
/ metabolism
Mice, Inbred C57BL
Myocardium
/ pathology
Paracrine Communication
/ drug effects
Transforming Growth Factor beta1
/ pharmacology
aging
autophagy
bone marrow
fibroblasts
secretome
Journal
Aging
ISSN: 1945-4589
Titre abrégé: Aging (Albany NY)
Pays: United States
ID NLM: 101508617
Informations de publication
Date de publication:
04 06 2021
04 06 2021
Historique:
received:
12
01
2021
accepted:
14
05
2021
pubmed:
6
6
2021
medline:
22
7
2021
entrez:
5
6
2021
Statut:
ppublish
Résumé
Bone marrow mononuclear cell therapy improves cardiac repair after myocardial infarction (MI), in-part through signaling to resident cardiac cells, such as fibroblasts, which regulate scar formation. The efficacy of cell therapy declines with age, as aging of both donor and recipient cells decreases repair responses. Autophagy regulates the microenvironment by both extracellular vesicle (EV)-dependent and independent secretion pathways. We hypothesized that age-related autophagy changes in bone marrow cells (BMCs) alter paracrine signaling, contributing to lower cell therapy efficacy. Here, we demonstrate that young Sca-1
Identifiants
pubmed: 34088884
pii: 203127
doi: 10.18632/aging.203127
pmc: PMC8221303
doi:
Substances chimiques
Antigens, Ly
0
Culture Media, Conditioned
0
Ly6a protein, mouse
0
Membrane Proteins
0
Transforming Growth Factor beta1
0
Autophagy-Related Protein 7
EC 6.2.1.45
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
14687-14708Subventions
Organisme : CIHR
ID : 332652
Pays : Canada
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