INT184222
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Although we did not investigate actin stress fiber formation in the present study, they are usually more pronounced in fibroblastic cells and have been shown to suppress SOX9 mRNA levels in chondrocytes [50]. | |||||||||||||||
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Interestingly, while the SOX9 dependency of COL2A1 expression has been unequivocally shown, it may not actually be a key regulator of COL2A1 promoter activity in human adult articular chondrocytes [82]. | |||||||||||||||
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Gruber et al considered that loss of expression of Sox9 in some of the anulus cell population may play a role in disc aging and degeneration, possibly by decreased modulation of the expression and production of Type II collagen of disc cells 36. | |||||||||||||||
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In the developing brain it is expressed in neural crest cells; the very same cells that differentiate into meninges, and animal studies have shown that inactivation of SOX9 in these cells results in craniofacial maldevelopment [25]. | |||||||||||||||
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SOX6 (usually in combination with SOX9, which was also decreased by IL-1 [albeit not significantly] in this study) determines the chondrogenic phenotype [52]. | |||||||||||||||
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The importance of IL-1 is reinforced by the fact that it has been shown to inhibit chondrogenesis in chondrogenic cells in vitro by downregulation of chondrocyte differentiation state marker genes, such as those encoding SOX9, collagen type II and others, while upregulating NO, prostaglandin E2 and MMP-3, and the finding that the effects could be inhibited by the addition of the IL-1 receptor antagonist (IL-1Ra) [179-181]. | |||||||||||||||
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IL-1 treatment of cells derived from non-degenerate discs resulted in a decrease in both SOX6 and SOX9 gene expression. | |||||||||||||||
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activation is associated with dedifferentiation and/or COX-2 expression and PGE2 production. 15d-PGJ2-induced inhibition of type II collagen and SOX-9 expression was prevented by the addition of 10 µM BADGE (bisphenol A diglycidyl ether, PPAR-? | |||||||||||||||
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