Protective Effects of Vitamin D on Proteoglycans of Human Articular Chondrocytes through TGF-β1 Signaling.
Humans
Chondrocytes
/ metabolism
Signal Transduction
/ drug effects
Transforming Growth Factor beta1
/ metabolism
Aggrecans
/ metabolism
Tumor Necrosis Factor-alpha
/ metabolism
Vitamin D
/ pharmacology
Proteoglycans
/ metabolism
Cartilage, Articular
/ metabolism
Cells, Cultured
Cell Survival
/ drug effects
Osteoarthritis
/ metabolism
Receptor, Transforming Growth Factor-beta Type I
/ metabolism
Receptors, Calcitriol
/ metabolism
TGF-β1 signaling
TNF-α
osteoarthritis
proteoglycan
vitamin D
Journal
Nutrients
ISSN: 2072-6643
Titre abrégé: Nutrients
Pays: Switzerland
ID NLM: 101521595
Informations de publication
Date de publication:
04 Sep 2024
04 Sep 2024
Historique:
received:
04
08
2024
revised:
23
08
2024
accepted:
03
09
2024
medline:
14
9
2024
pubmed:
14
9
2024
entrez:
14
9
2024
Statut:
epublish
Résumé
The extracellular matrix of cartilage primarily constitutes of collagen and aggrecan. Cartilage degradation starts with aggrecan loss in osteoarthritis (OA). Vitamin D (VD) plays an essential role in several inflammation-related diseases and can protect the collagen in cartilage during OA. The present study focused on the role of VD in aggrecan turnover of human articular chondrocytes treated with tumor necrosis factor α (TNF-α) and the possible mechanism. Treatment with different doses of VD and different periods of intervention with TNF-α and TGF-β1 receptor (TGFβR1) inhibitor SB525334 were investigated. The viability of human chondrocytes and extracellular secretion of TGF-β1 were measured. The expression of intracellular TGFβR1 and VD receptor was examined. Transcriptional and translational levels of aggrecan and the related metabolic factors were analyzed. The results showed that TNF-α markedly reduced the viability, TGFβR1 expressions and aggrecan levels of human chondrocytes, and increased disintegrin and metalloproteinase with thrombospondin motifs. The alterations were partially inhibited by VD treatment. Furthermore, the effects of VD were blocked by the TGFβR1 inhibitor SB525334 in TNF-α-treated cells. VD may prevent proteoglycan loss due to TNF-α via TGF-β1 signaling in human chondrocytes.
Identifiants
pubmed: 39275306
pii: nu16172991
doi: 10.3390/nu16172991
pii:
doi:
Substances chimiques
Transforming Growth Factor beta1
0
Aggrecans
0
Tumor Necrosis Factor-alpha
0
Vitamin D
1406-16-2
Proteoglycans
0
TGFB1 protein, human
0
Receptor, Transforming Growth Factor-beta Type I
EC 2.7.11.30
TGFBR1 protein, human
EC 2.7.11.30
Receptors, Calcitriol
0
ACAN protein, human
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : National Natural Science Foundation of China
ID : 12172011
Organisme : National Natural Science Foundation of China
ID : 11872076