Selenium Nanoparticles by Moderating Oxidative Stress Promote Differentiation of Mesenchymal Stem Cells to Osteoblasts.
Adipogenesis
/ drug effects
Cell Differentiation
/ drug effects
Cells, Cultured
Extracellular Signal-Regulated MAP Kinases
/ metabolism
Humans
JNK Mitogen-Activated Protein Kinases
/ metabolism
MAP Kinase Signaling System
/ drug effects
Mesenchymal Stem Cells
/ cytology
Nanoparticles
Osteoblasts
/ cytology
Osteogenesis
/ drug effects
Oxidative Stress
/ drug effects
Selenium
/ chemistry
p38 Mitogen-Activated Protein Kinases
/ metabolism
antioxidant
osteogenic differentiation
selenium nanoparticles stem cells
Journal
International journal of nanomedicine
ISSN: 1178-2013
Titre abrégé: Int J Nanomedicine
Pays: New Zealand
ID NLM: 101263847
Informations de publication
Date de publication:
2021
2021
Historique:
received:
07
10
2020
accepted:
27
11
2020
entrez:
25
1
2021
pubmed:
26
1
2021
medline:
28
1
2021
Statut:
epublish
Résumé
Redox homeostasis plays an important role in the osteogenic differentiation of human mesenchymal stem cells (hMSCs) for bone engineering. Oxidative stress (OS) is believed to induce osteoporosis by changing bone homeostasis. Selenium nanoparticles (SeNPs), an antioxidant with pleiotropic pharmacological activity, prevent bone loss. However, the molecular mechanism underlying the osteogenic activity during hMSC-SeNP interaction is unclear. This study assessed the effects of different concentrations (25, 50, 100, and 300 ng/mL) of SeNPs on the cell viability and differentiation ability of human embryonic stem cell-derived hMSCs. In addition, we analyzed OS markers and their effect on mitogen-activated protein kinase (MAPK) and Forkhead box O3 (FOXO3) during osteogenesis. SeNPs increased the cell viability of hMSCs and induced their differentiation toward an osteogenic over an adipogenic lineage by enhancing osteogenic transcription and mineralization, while inhibiting Nile red staining and adipogenic gene expression. By preventing excessive reactive oxygen species accumulation, SeNPs increased antioxidant levels in hMSCs undergoing osteogenesis compared to untreated cells. In addition, SeNPs significantly upregulated the gene and protein expression of phosphorylated c-Jun N-terminal kinase (JNK) and FOXO3a, with no significant change in the expression levels of extracellular signal-related kinase (ERK) and p38 MAPK. The results approved that low concentrations of SeNPs might enhance the cell viability and osteogenic potential of hMSCs by moderating OS. Increased JNK and FOXO3a expression shows that SeNPs might enhance osteogenesis via activation of the JNK/FOXO3 pathway. In addition, SeNP co-supplementation might prevent bone loss by enhancing osteogenesis and, thus, can be an effective candidate for treating osteoporosis through cell-based therapy.
Identifiants
pubmed: 33488075
doi: 10.2147/IJN.S285233
pii: 285233
pmc: PMC7814244
doi:
Substances chimiques
Extracellular Signal-Regulated MAP Kinases
EC 2.7.11.24
JNK Mitogen-Activated Protein Kinases
EC 2.7.11.24
p38 Mitogen-Activated Protein Kinases
EC 2.7.11.24
Selenium
H6241UJ22B
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
331-343Informations de copyright
© 2021 Fatima et al.
Déclaration de conflit d'intérêts
The authors report no conflicts of interest in this work.
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