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Effect of miR‑21 in mesenchymal stem cells‑derived extracellular vesicles behavior

Authors :
Xunta de Galicia
Ministerio de Ciencia e Innovación (España)
Universidad de La Coruña
Instituto de Salud Carlos III
European Commission
Morente-López, Miriam
Mato-Basalo, Rocío
Lucio-Gallego, Sergio
Gil, Concha
Carrera, Mónica
Fafián-Labora, Juan
Mateos, Jesús
Arufe, María C.
Xunta de Galicia
Ministerio de Ciencia e Innovación (España)
Universidad de La Coruña
Instituto de Salud Carlos III
European Commission
Morente-López, Miriam
Mato-Basalo, Rocío
Lucio-Gallego, Sergio
Gil, Concha
Carrera, Mónica
Fafián-Labora, Juan
Mateos, Jesús
Arufe, María C.
Publication Year :
2023

Abstract

[Background] A challenging new branch of research related to aging-associated diseases is the identification of miRNAs capable of modulating the senescence-associated secretory phenotype (SASP) which characterizes senescent cells and contributes to driving inflammation. [Methods] Mesenchymal stem cells (MSC) from human umbilical cord stroma were stable modified using lentivirus transduction to inhibit miR-21-5p and shotgun proteomic analysis was performed in the MSC-derived extracellular vesicles (EV) to check the effect of miR-21 inhibition in their protein cargo. Besides, we studied the paracrine effect of those modified extracellular vesicles and also their effect on SASP. [Results] Syndecan-1 (SDC1) was the most decreased protein in MSC-miR21−-derived EV, and it was involved in inflammation and EV production. MSC-miR21−-derived EV were found to produce a statistically significant inhibitory effect on SASP and inflammaging markers expression in receptor cells, and in the opposite way, these receptor cells increased their SASP and inflammaging expression statistically significantly when treated with MSC-miR-21+-derived EV. [Conclusion] This work demonstrates the importance of miR-21 in inflammaging and its role in SASP through SDC1

Details

Database :
OAIster
Notes :
English
Publication Type :
Electronic Resource
Accession number :
edsoai.on1431963571
Document Type :
Electronic Resource