Proinflammatory effects of IL-1β combined with IL-17A promoted cartilage degradation and suppressed genes associated with cartilage matrix synthesis in vitro
© 2019 by the authors. Combinations of IL-1β and other proinflammatory cytokines reportedly promote the severity of arthritis. We aimed to investigate the effects of IL-1β combined with IL-17A on cartilage degradation and synthesis in in vitro models. Cartilage explant degradation was determined usi...
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th-cmuir.6653943832-676102020-04-02T15:17:21Z Proinflammatory effects of IL-1β combined with IL-17A promoted cartilage degradation and suppressed genes associated with cartilage matrix synthesis in vitro Patiwat Kongdang Chatchadawalai Chokchaitaweesuk Siriwan Tangyuenyong Siriwan Ongchai Biochemistry, Genetics and Molecular Biology Chemistry Pharmacology, Toxicology and Pharmaceutics © 2019 by the authors. Combinations of IL-1β and other proinflammatory cytokines reportedly promote the severity of arthritis. We aimed to investigate the effects of IL-1β combined with IL-17A on cartilage degradation and synthesis in in vitro models. Cartilage explant degradation was determined using sulfated glycosaminoglycans (S-GAGs) levels, matrix metalloproteinase (MMP13) gene expression, uronic acid, and collagen contents. Cell morphology and accumulation of proteoglycans were evaluated using hematoxylin-eosin and safranin O staining, respectively. In the pellet culture model, expressions of cartilage-specific anabolic and catabolic genes were evaluated using real-time qRT-PCR. Early induction of MMP13 gene expression was found concomitantly with significant S-GAGs release. During the prolonged period, S-GAGs release was significantly elevated, while MMP-13 enzyme levels were persistently increased together with the reduction of the cartilaginous matrix molecules. The pellet culture showed anabolic gene downregulation, while expression of the proinflammatory cytokines, mediators, and MMP13 genes were elevated. After cytokine removal, these effects were restored to nearly basal levels. This study provides evidence that IL-1β combined with IL-17A promoted chronic inflammatory arthritis by activating the catabolic processes accompanied with the suppression of cartilage anabolism. These suggest that further applications, which suppress inflammatory enhancers, especially IL-17A, should be considered as a target for arthritis research and therapy. 2020-04-02T14:56:34Z 2020-04-02T14:56:34Z 2019-10-13 Journal 14203049 2-s2.0-85073446046 10.3390/molecules24203682 https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85073446046&origin=inward http://cmuir.cmu.ac.th/jspui/handle/6653943832/67610 |
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Biochemistry, Genetics and Molecular Biology Chemistry Pharmacology, Toxicology and Pharmaceutics Patiwat Kongdang Chatchadawalai Chokchaitaweesuk Siriwan Tangyuenyong Siriwan Ongchai Proinflammatory effects of IL-1β combined with IL-17A promoted cartilage degradation and suppressed genes associated with cartilage matrix synthesis in vitro |
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© 2019 by the authors. Combinations of IL-1β and other proinflammatory cytokines reportedly promote the severity of arthritis. We aimed to investigate the effects of IL-1β combined with IL-17A on cartilage degradation and synthesis in in vitro models. Cartilage explant degradation was determined using sulfated glycosaminoglycans (S-GAGs) levels, matrix metalloproteinase (MMP13) gene expression, uronic acid, and collagen contents. Cell morphology and accumulation of proteoglycans were evaluated using hematoxylin-eosin and safranin O staining, respectively. In the pellet culture model, expressions of cartilage-specific anabolic and catabolic genes were evaluated using real-time qRT-PCR. Early induction of MMP13 gene expression was found concomitantly with significant S-GAGs release. During the prolonged period, S-GAGs release was significantly elevated, while MMP-13 enzyme levels were persistently increased together with the reduction of the cartilaginous matrix molecules. The pellet culture showed anabolic gene downregulation, while expression of the proinflammatory cytokines, mediators, and MMP13 genes were elevated. After cytokine removal, these effects were restored to nearly basal levels. This study provides evidence that IL-1β combined with IL-17A promoted chronic inflammatory arthritis by activating the catabolic processes accompanied with the suppression of cartilage anabolism. These suggest that further applications, which suppress inflammatory enhancers, especially IL-17A, should be considered as a target for arthritis research and therapy. |
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Patiwat Kongdang Chatchadawalai Chokchaitaweesuk Siriwan Tangyuenyong Siriwan Ongchai |
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Patiwat Kongdang Chatchadawalai Chokchaitaweesuk Siriwan Tangyuenyong Siriwan Ongchai |
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Patiwat Kongdang |
title |
Proinflammatory effects of IL-1β combined with IL-17A promoted cartilage degradation and suppressed genes associated with cartilage matrix synthesis in vitro |
title_short |
Proinflammatory effects of IL-1β combined with IL-17A promoted cartilage degradation and suppressed genes associated with cartilage matrix synthesis in vitro |
title_full |
Proinflammatory effects of IL-1β combined with IL-17A promoted cartilage degradation and suppressed genes associated with cartilage matrix synthesis in vitro |
title_fullStr |
Proinflammatory effects of IL-1β combined with IL-17A promoted cartilage degradation and suppressed genes associated with cartilage matrix synthesis in vitro |
title_full_unstemmed |
Proinflammatory effects of IL-1β combined with IL-17A promoted cartilage degradation and suppressed genes associated with cartilage matrix synthesis in vitro |
title_sort |
proinflammatory effects of il-1β combined with il-17a promoted cartilage degradation and suppressed genes associated with cartilage matrix synthesis in vitro |
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2020 |
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https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85073446046&origin=inward http://cmuir.cmu.ac.th/jspui/handle/6653943832/67610 |
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