LPS‑mediated adaptation accelerates ecto‑MSCs differentiation into osteoblasts.
Humans
Mesenchymal Stem Cells
/ metabolism
Cell Differentiation
/ drug effects
Osteoblasts
/ metabolism
Lipopolysaccharides
/ pharmacology
Osteogenesis
/ drug effects
Cells, Cultured
Alkaline Phosphatase
/ metabolism
Interleukin-10
/ metabolism
Nasal Mucosa
/ cytology
Bone Regeneration
/ drug effects
IL‑10
ecto‑MSCs
lipopolysa ccharide
osteogenic differentiation
Journal
Molecular medicine reports
ISSN: 1791-3004
Titre abrégé: Mol Med Rep
Pays: Greece
ID NLM: 101475259
Informations de publication
Date de publication:
Dec 2024
Dec 2024
Historique:
received:
05
03
2024
accepted:
10
09
2024
medline:
18
10
2024
pubmed:
18
10
2024
entrez:
18
10
2024
Statut:
ppublish
Résumé
Addressing the repair and regeneration of large bone defects poses significant challenges in bone tissue engineering. Despite the abundant evidence demonstrating the positive role of MSCs in osteogenesis, their limited osteogenic differentiation ability still needs to be improved. The present study used lipopolysaccharide (LPS) to enhance the osteogenic properties of ecto‑mesenchymal stem cells (EMSCs). Human nasal respiratory mucosa‑derived EMSCs were cultured on plates and stimulated with LPS for 5 days prior to undergoing osteogenic differentiation. The findings revealed that LPS effectively stimulated the osteogenic differentiation capacity of EMSCs, as evidenced by heightened alkaline phosphatase activity, elevated expression levels of osteogenic‑related proteins and enhanced mineralization of EMSCs. The present study also demonstrated that the augmentation occurred due to increased IL‑10 levels, although it was not solely attributable to this factor. Together, the findings illustrated that the LPS‑mediated adaptation of EMSCs is an active process driving osteogenic differentiation and could be a novel strategy for bone regeneration.
Identifiants
pubmed: 39422037
doi: 10.3892/mmr.2024.13365
pii: 241
doi:
pii:
Substances chimiques
Lipopolysaccharides
0
Alkaline Phosphatase
EC 3.1.3.1
Interleukin-10
130068-27-8
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM