About: The JNK pathway represents a novel target in the treatment of rheumatoid arthritis through the suppression of MMP-3

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About: The JNK pathway represents a novel target in the treatment of rheumatoid arthritis through the suppression of MMP-3 Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	The JNK pathway represents a novel target in the treatment of rheumatoid arthritis through the suppression of MMP-3
Creator	Endo, Naoto Kanai, Tomotake Kawashima, Hiroyuki Kijima, Yasufumi Kondo, Naoki Ogose, Akira Okada, Masayasu Okumura, Go Sano, Hiroshige
source	PMC
abstract	BACKGROUND AND AIM: The pathophysiology of rheumatoid arthritis (RA) is characterized by excess production of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) by neutrophils and macrophages in synovium. Additionally, these cytokines promote the production of reactive oxygen species (ROS), and increased production of matrix metalloproteinases (MMPs), including MMP-3, in synoviocytes that result in joint destruction. There is limited information on how proteolytic enzymes such as MMP-3 can be regulated. We evaluated the effect of the antioxidant N-acetylcysteine (NAC) on RA and identified the relationship between the c-Jun N terminal kinase (JNK) pathway and MMP-3. We hypothesized that elucidating this relationship would lead to novel therapeutic approaches to RA treatment and management. METHODS: We investigated the effect of administering a low dose (1000 μM or less) of an antioxidant (NAC) to human rheumatoid fibroblast-like synoviocytes (MH7A cells). We also investigated the response of antioxidant genes such as nuclear factor erythroid -derived 2-related factor 2 (Nrf2) and Sequestosome 1 (p62). The influence of MMP-3 expression on the JNK pathway leading to joint destruction and the mechanisms underlying this relationship were investigated through primary dispersion culture cells collected from the synovial membranes of RA patients, consisting of rheumatoid arthritis-fibroblast-like synoviocytes (RA-FLS). RESULTS: Low-dose NAC (1000 μM) increased the expression of Nrf2 and phospho-p62 in MH7A cells, activating antioxidant genes, suppressing the expression of MMP-3, and inhibiting the phosphorylation of JNK. ROS, MMP-3 expression, and IL-6 was suppressed by administering 30 μM of SP600125 (a JNK inhibitor) in MH7A cells. Furthermore, the administration of SP600125 (30 μM) to RA-FLS suppressed MMP-3. CONCLUSIONS: We demonstrated the existence of an MMP-3 suppression mechanism that utilizes the JNK pathway in RA-FLS. We consider that the JNK pathway could be a target for future RA therapies.
has issue date	2020-07-17(xsd:dateTime)
bibo:doi	10.1186/s13018-020-01595-9
bibo:pmid	32131874
has license	cc-by
sha1sum (hex)	a02dfce327159899d4256cf60c95f4884c0ad170
schema:url	https://doi.org/10.1186/s13018-020-01595-9
resource representing a document's title	The JNK pathway represents a novel target in the treatment of rheumatoid arthritis through the suppression of MMP-3
has PubMed Central identifier	PMC7371465
has PubMed identifier	32131874
schema:publication	J Orthop Surg Res
resource representing a document's body	covid:a02dfce327159899d4256cf60c95f4884c0ad170#body_text
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