INT217742
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
It did not upregulate chondrocyte proliferation and type II collagen synthesis as evidenced by the lack of significant changes in the expression of cyclin B2 and COL2A1, respectively. | |||||||||||||||
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generation [33], to stimulate collagen and proteoglycan synthesis [11-13] and chondrocyte proliferation [11], and to inhibit chondrocyte terminal differentiation/hypertrophy [24,25] and apoptosis in endothelial cells [34]. | |||||||||||||||
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This involves phenotypic hypertrophy-related changes in chondrocytes, such as the production of type X collagen (COL10A1) (hypertrophy marker), and the upregulation of collagenase matrix metalloproteinase (MMP)-13, as is seen in the fetal growth plate [1-3]. | |||||||||||||||
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In the present article we report that physiological tonicity (380 mOsm) during isolation and monolayer expansion can suppress chondrocyte dedifferentiation and that expression of the extracelluar matrix components collagen type I and collagen type II as well as aggrecan is NFAT5 dependent. | |||||||||||||||
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Aigner and colleagues have suggested that the expression of COL2A1 is suppressed in the upper zones of early OA cartilage, but increased in late-stage OA cartilage relative to normal controls [31], [32]. | |||||||||||||||
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Controversy exists among others about whether COL2A1 expression is increased or suppressed in OA cartilage. | |||||||||||||||
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They used adenoviral delivery vectors expressing Sox9 to infect a chondroblastic cell line and human disc cells; Sox9 and Type II collagen production increased. | |||||||||||||||
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However, there were small, but significant, increases in gene expression for COL2A1 and ACAN in AC cells when compared with NP cells (P = 0.011 and 0.026, respectively; Figure 2). | |||||||||||||||
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Aggrecan and collagen type-II gene expression, which is characteristic for hyaline cartilage, stayed elevated, while expression of the collagen type-I gene, indicating dedifferentiated chondrocytes, was slowly decreasing during cultivation. | |||||||||||||||
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Gene expression of collagen type-II, collagen type-I, aggrecan, MMP-13, IL-6, Il-1? | |||||||||||||||
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In one of these clinical studies, progression was identified by the increase in type II collagen cleavage products compared to a decrease in the propeptide marker of synthesis [2]. | |||||||||||||||
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Studies using explants of human cartilage indicate that catabolic degradation of cartilage matrix, a MMP dependent response, is suppressed by reparagen in concert with increased expression of the cartilage repair factor, IGF-1 [20]. | |||||||||||||||
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Collagen type II expression in MPCs was low and found to be only increased in the presence of 10 and 20 ? | |||||||||||||||
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For the 7-day and 10-day culture periods, a progressive stimulation of collagen type II synthesis was observed with PPS concentrations up to 5 ? | |||||||||||||||
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Reparagen is derived from South American medicinal plants and supported by preclinical studies demonstrating chondroprotective, cytoprotective, and anti-inflammatory properties [21-24] as well as the ability to enhance human chondrocyte production of the cartilage repair factor, IGF-1 [20]. | |||||||||||||||
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The aforementioned findings were consistent with the real-time PCR results, which showed the corresponding upregulation of SOX-9, aggrecan and type II collagen gene expression but downregulation of type I collagen expression by MPCs cultured in the presence of PPS. | |||||||||||||||
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In the 5-day cultures, lower but significant (P < 0.001 to 0.05) stimulation of collagen type II synthesis by MPCs was still evident at PPS concentrations up to 20 ? | |||||||||||||||
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synthesis, and enhances type II collagen and aggrecan core protein synthesis in human articular chondrocytes [24]. | |||||||||||||||
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For instance, treatment with PGD2 enhances the expression of the cartilage-specific matrix components collagen type II and aggrecan [7] and prevents chondrocyte apoptosis [8]. | |||||||||||||||
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It stimulates collagen type II and proteoglycan expression, inhibits MMP, proinflammatory cytokine or nitric oxide expression and protects against chondrocyte apoptosis (reviewed in [71]). | |||||||||||||||
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