In vivo experiments using surgically-induced OA rats showed <sub>MC</sub> SOX9/6/shANG-tADSC-treated rats had significantly lower levels of cyclooxygenase (COX-2) and MMP13 in synovial fluids than <sub>MC</sub> SOX9/6-tADSC-treated rats, but no significant difference was observed between them in histological appearances.
Human chondrocyte cell lines, CHON-001 and ATDC5, were treated with different doses of interleukin-1β (IL-1β) to simulate the inflammatory response environment of OA. miR-138-5p mimics, miR-138-5p inhibitors and SOX9 small interfering RNA (siRNA) were constructed and transfected into CHON-001 and ATDC5 cells.
When locally administered in vivo in an OA mouse model, the hydrogels demonstrated the ability to restore, to some extent, bone remineralization, proteoglycan production, levels of Sox-9 and Runx-2.
While H-PRP showed similar effects on expression of chondrogenic markers (Col2a1 and Sox9) as the negative control group (p > 0.05), OA-PRP decreased chondrocyte expression of Col2a1 and Sox-9 messenger RNA by 40% and 30%, respectively (Col2a1, p = 0.015; Sox9, p = 0.037).
Moreover, the G allele of the polymorphism rs12601701 and the A allele of the polymorphism rs1042667 could significantly elevate the risk of OA (OR = 2.075, 95%CI = 1.021-4.218).SOX9 polymorphism rs1042667 may be a risk factor for OA in Chinese Han population.
Both peptides, however, reversed the downregulation of SOX9 and aggrecan (ACAN), and decrease of COL10A1 gene expression in preserved human OA cartilage explants.
This study aimed to determine the collagen type II (COL2) and SOX9 expression in interleukin growth factor (IGF-1)-induced Wharton's Jelly mesenchymal stem cells (WJMSCs) and the level of chondrogenic markers in co-culture IGF1-WJMSCs and IL1β-CHON002 as osteoarthritis (OA) cells model.
There was a significant reduction in miR-140 and SOX9 expression in OA groups compared to the normal group, and there was a further reduction in the severe OA group compared to the moderate OA group.
PSMD11 gain-of- function by transfection increased proteasomal function, increased levels of SOX9-induced AGC1 mRNA, stimulated elements of the autophagic machinery, and inhibited extracellular levels of interleukin-1-induced NO and matrix metalloproteinase 13 in OA chondrocytes.
Cartilage degeneration in OA is a gradual progress accompanied with gradual loss of collagen type II and a gradual decrease in mRNA expression of SOX9, ACAN and COL2A1.
miR-30a was significantly upregulated and Sox9 was downregulated in primary chondrocytes from cartilage taken from OA donors compared to healthy controls.
There was a significant increase in H3K9 and H3K27 trimethylation and a significant decrease in the acetylation of H3K9, 15, 18, 23, and 27 at SOX-9 promoters in OA chondrocytes.
Thus, we conclude that co-expression of the α2M and Sox9 genes, combined with chitosan‑mediated gene delivery, will offer potential as a novel means by which to treat OA via intra-articular injection.
We confirmed that SOX9 is an ERRα target gene in human, as in rodent, chondrocytes and identified MMP-13 as a potential new target gene, which suggests that ERRα may both respond to the healing signal and contribute to extracellular degradation in OA cartilage.
SOX-5, SOX-6, and SOX-9 gene expressions significantly decreased by 41% (p = 0.047), 46% (p = 0.047), and 56% (p = 0.029) in advanced OA area compared with the minimally OA area.
SOX9 (38-fold) and aggrecan (4-fold) gene expression were both lower in OA (p<0.001), and collagen I (17-fold) and II (2.5-fold) gene expression were each increased in a subset of OA samples.