Exosomes derived from miRNA-210 overexpressing bone marrow mesenchymal stem cells protect lipopolysaccharide induced chondrocytes injury via the NF-κB pathway.
Bone mesenchymal stem cells
Chondrocytes
Exosomes
NF-κB
miRNA-210
Journal
Gene
ISSN: 1879-0038
Titre abrégé: Gene
Pays: Netherlands
ID NLM: 7706761
Informations de publication
Date de publication:
15 Aug 2020
15 Aug 2020
Historique:
received:
01
01
2020
revised:
30
04
2020
accepted:
11
05
2020
pubmed:
20
5
2020
medline:
23
6
2020
entrez:
20
5
2020
Statut:
ppublish
Résumé
Bone marrow mesenchymal stem cells (BMSCs)-derived exosomes (Exos) have anti-inflammatory and anti-apoptotic functions. miRNA-210 has also been confirmed to play a role in inhibiting proinflammatory cytokines. Herein, we aimed to explore the effects of Exos derived from miRNA-210-overexpressing BMSCs (BMSCs-210-Exos) and the mechanisms by which they provide protection to chondrocytes from lipopolysaccharide (LPS)-induced injury. BMSCs were transfected with or without miRNA-210. Exos substantially improved the proliferation of chondrocytes and inhibited LPS-induced cell apoptosis. Furthermore, BMSCs-210-Exos promoted the proliferation of chondrocytes and prevented LPS-induced cell apoptosis better than BMSCs-Exos not overexpressing miRNA-210. In addition, tumor necrosis factor receptor superfamily member 21 (Tnfrsf21) expression was inhibited and the NF-κB pathway was attenuated by both BMSCs-Exos and BMSCs-210-Exos during LPS-induced chondrocyte injury. Collectively, these results suggest that BMSCs-210-Exos enhance the protection of chondrocytes from LPS-induced injury via the NF-κB pathway.
Identifiants
pubmed: 32428694
pii: S0378-1119(20)30433-9
doi: 10.1016/j.gene.2020.144764
pii:
doi:
Substances chimiques
Lipopolysaccharides
0
MicroRNAs
0
NF-kappa B
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
144764Informations de copyright
Copyright © 2020 Elsevier B.V. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.