Please use this identifier to cite or link to this item: http://cmuir.cmu.ac.th/jspui/handle/6653943832/67610
Title: Proinflammatory effects of IL-1β combined with IL-17A promoted cartilage degradation and suppressed genes associated with cartilage matrix synthesis in vitro
Authors: Patiwat Kongdang
Chatchadawalai Chokchaitaweesuk
Siriwan Tangyuenyong
Siriwan Ongchai
Keywords: Biochemistry, Genetics and Molecular Biology
Chemistry
Pharmacology, Toxicology and Pharmaceutics
Issue Date: 13-Oct-2019
Abstract: © 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.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85073446046&origin=inward
http://cmuir.cmu.ac.th/jspui/handle/6653943832/67610
ISSN: 14203049
Appears in Collections:CMUL: Journal Articles

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