Regulation of Xylosyltransferase I Gene Expression by Interleukin 1β in Human Primary Chondrocyte Cells

Khair, Mostafa; Bourhim, Mustapha; Barré, Lydia; Liu, Dong; Netter, Patrick; Magdalou, Jacques; Fournel‐Gigleux, Sylvie; Ouzzine, Mohamed

doi:10.1074/jbc.m112.419887

Cited by 21 publications

(33 citation statements)

References 40 publications

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“…As a typical pro-inflammatory factor in OA pathophysiology, IL-1β could inhibit synthesis of GAG due to decrease gene expression and enzyme activity of GTs [23], [24]. On the contrary, IGF-1 is one of the key protective factors of cartilage.…”

Section: Introductionmentioning

confidence: 99%

Angelica Sinensis Polysaccharides Stimulated UDP-Sugar Synthase Genes through Promoting Gene Expression of IGF-1 and IGF1R in Chondrocytes: Promoting Anti-Osteoarthritic Activity

Wen

Tan

et al. 2014

PLoS ONE

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BackgroundOsteoarthritis (OA) is a chronic joints disease characterized by progressive degeneration of articular cartilage due to the loss of cartilage matrix. Previously, we found, for the first time, that an acidic glycan from Angelica Sinensis Polysaccharides (APSs), namely the APS-3c, could protect rat cartilage from OA due to promoting glycosaminoglycan (GAG) synthesis in chondrocytes. In the present work, we tried to further the understanding of ASP-3c’s anti-OA activity.Methodology/Principal FindingsHuman primary chondrocytes were treated with APS-3c or/and recombinant human interleukin 1β (IL-1β). It turned out that APS-3c promoted synthesis of UDP-xylose and GAG, as well as the gene expression of UDP-sugar synthases (USSs), insulin like growth factor 1 (IGF1) and IGF1 receptor (IGF1R), and attenuated the degenerative phenotypes, suppressed biosynthesis of UDP-sugars and GAG, and inhibited the gene expression of USSs, IGF1 and IGF1R induced by IL-1β. Then, we induced a rat OA model with papain, and found that APS-3c also stimulated GAG synthesis and gene expression of USSs, IGF1 and IGF1R in vivo. Additionally, recombinant human IGF1 and IGF1R inhibitor NP-AEW541 were applied to figure out the correlation between stimulated gene expression of USSs, IGF1 and IGF1R induced by APS-3c. It tuned out that the promoted GAG synthesis and USSs gene expression induced by APS-3c was mediated by the stimulated IGF1 and IGF1R gene expression, but not through directly activation of IGF1R signaling pathway.Conclusions/SignificancesWe demonstrated for the first time that APS-3c presented anti-OA activity through stimulating IGF-1 and IGF1R gene expression, but not directly activating the IGF1R signaling pathway, which consequently promoted UDP-sugars and GAG synthesis due to up-regulating gene expression of USSs. Our findings presented a better understanding of APS-3c’s anti-OA activity and suggested that APS-3c could potentially be a novel therapeutic agent for OA.

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Section: Introductionmentioning

confidence: 99%

Angelica Sinensis Polysaccharides Stimulated UDP-Sugar Synthase Genes through Promoting Gene Expression of IGF-1 and IGF1R in Chondrocytes: Promoting Anti-Osteoarthritic Activity

Wen

Tan

et al. 2014

PLoS ONE

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“…TNF-α also suppresses bone formation via increased osteoblast apoptosis [24], and reduced differentiation and proliferation of osteoblasts and their progenitors [25]. IL-1β reduces chondrocyte proteoglycan synthesis [26], increases the synthesis of matrix metalloproteinases and the release of nitric oxide [27]. Transgenic mice deficient in IL-1 receptor antagonist spontaneously develop a chronic arthritis similar to RA with bone erosions and present higher susceptibility for collagen-induced arthritis [28].…”

Section: Discussionmentioning

confidence: 99%

Ameliorative effect and potential mechanism of Ermiao san on adjuvant-induced arthritis in rats

Chen¹,

Feng²

2016

Trop. J. Pharm Res

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“…Attention was particularly paid to glycosyltransferases involved in the tetrasaccharide linkage region, especially, β1,3-glucuronosyltransferase 1 and xyloxyltransferase-1 as their expression level was particularly depressed during OA or after addition of IL-1β on chondrocytes [3,31], thus explaining the decrease in the content of proteoglycans in cartilage [32].…”

Section: Polysaccharides From Angelica Sinensis Promote Proteoglycan mentioning

confidence: 99%

Angelica sinensis and osteoarthritis: A natural therapeutic link?

Magdalou

Chen

Wang

et al. 2015

Bio-Medical Materials and Engineering

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The dried root of Angelica sinensis is widely used in Chinese traditional medicine for its beneficial effects against several diseases, including osteoarthritis. In order to understand the mechanism of action, two main components of the plant, the phytochemical, sodium ferulate, and a polysaccharidic fraction have been tested on osteoarthritis animal models or in human chondrocytes stimulated by the pro-inflammatory cytokine, Interleukine-1β. The results showed that sodium ferulate exhibited marked anti-inflammatory and anti-apoptotic properties by inhibiting the TNF/TNFR signal transduction pathway. On the other hand, the polysaccharidic fraction which contains a mixture of various carbohydrates was found to promote proteoglycan biosynthesis in cartilage matrix by stimulating the activity of the UDP-glycosyltransferases that synthesize the chondroitin sulfate chains of aggrecans. It is suggested that the combined action of sodium ferulate and polysaccharidic fraction would prevent cartilage destruction in osteoarthritis and favor cartilage repair.

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Regulation of Xylosyltransferase I Gene Expression by Interleukin 1β in Human Primary Chondrocyte Cells

Cited by 21 publications

References 40 publications

Angelica Sinensis Polysaccharides Stimulated UDP-Sugar Synthase Genes through Promoting Gene Expression of IGF-1 and IGF1R in Chondrocytes: Promoting Anti-Osteoarthritic Activity

Angelica Sinensis Polysaccharides Stimulated UDP-Sugar Synthase Genes through Promoting Gene Expression of IGF-1 and IGF1R in Chondrocytes: Promoting Anti-Osteoarthritic Activity

Ameliorative effect and potential mechanism of Ermiao san on adjuvant-induced arthritis in rats

Angelica sinensis and osteoarthritis: A natural therapeutic link?

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