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Role of high-temperature requirement serine protease A 2 in rheumatoid inflammation.
Jeong, Gi Heon; Nam, Min-Kyung; Hur, Wonhee; Heo, Seolhee; Lee, Saseong; Choi, Eunbyeol; Park, Jae Hyung; Park, Youngjae; Kim, Wan-Uk; Rhim, Hyangshuk; Yoo, Seung-Ah.
Afiliação
  • Jeong GH; Department of Biomedicine & Health Sciences, Department of Medical Life Sciences, College of Medicine, The Catholic University of Korea, Seoul, Korea.
  • Nam MK; Center for Integrative Rheumatoid Transcriptomics and Dynamics, The Catholic University of Korea, Seoul, Korea.
  • Hur W; Department of Biomedicine & Health Sciences, Department of Medical Life Sciences, College of Medicine, The Catholic University of Korea, Seoul, Korea.
  • Heo S; Division of Chronic Viral Diseases, Center for Emerging Virus Research, Korea National Institute of Health, Cheongju, Korea.
  • Lee S; Department of Biomedicine & Health Sciences, Department of Medical Life Sciences, College of Medicine, The Catholic University of Korea, Seoul, Korea.
  • Choi E; Center for Integrative Rheumatoid Transcriptomics and Dynamics, The Catholic University of Korea, Seoul, Korea.
  • Park JH; Center for Integrative Rheumatoid Transcriptomics and Dynamics, The Catholic University of Korea, Seoul, Korea.
  • Park Y; Department of Biomedicine & Health Sciences, Department of Medical Life Sciences, College of Medicine, The Catholic University of Korea, Seoul, Korea.
  • Kim WU; Center for Integrative Rheumatoid Transcriptomics and Dynamics, The Catholic University of Korea, Seoul, Korea.
  • Rhim H; School of Chemical Engineering, College of Engineering, Sungkyunkwan University, Suwon, Korea.
  • Yoo SA; Department of Internal Medicine, The Catholic University of Korea, Seoul, Korea.
Arthritis Res Ther ; 25(1): 96, 2023 06 07.
Article em En | MEDLINE | ID: mdl-37287073
BACKGROUND: High-temperature requirement serine protease A 2 (HtrA2) is known to be involved in growth, unfolded protein response to stress, apoptosis, and autophagy. However, whether HtrA2 controls inflammation and immune response remains elusive. METHODS: Expression of HtrA2 in the synovial tissue of patients was examined using immunohistochemistry and immunofluorescence staining. Enzyme-linked immunosorbent assay was used to determine the concentrations of HtrA2, interleukin-6 (IL-6), interleukin-8 (IL-8), chemokine (C-C motif) ligand 2 (CCL2), and tumor necrosis factor α (TNFα). Synoviocyte survival was assessed by MTT assay. For the downregulation of HtrA2 transcripts, cells were transfected with HtrA2 siRNA. RESULTS: We found that the concentration of HtrA2 was elevated in rheumatoid arthritis (RA) synovial fluid (SF) than in osteoarthritis (OA) SF, and its concentrations were correlated with the number of immune cells in the RA SF. Interestingly, HtrA2 levels in the SF of RA patients were elevated in proportion to synovitis severity and correlated with the expression of proinflammation cytokines and chemokines, such as IL-6, IL-8, and CCL2. In addition, HtrA2 was highly expressed in RA synovium and primary synoviocytes. RA synoviocytes released HtrA2 when stimulated with ER stress inducers. Knockdown of HtrA2 inhibited the IL1ß-, TNFα-, and LPS-induced release of proinflammatory cytokines and chemokines by RA synoviocytes. CONCLUSION: HtrA2 is a novel inflammatory mediator and a potential target for the development of an anti-inflammation therapy for RA.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Artrite Reumatoide / Sinoviócitos Limite: Humans Idioma: En Ano de publicação: 2023 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Artrite Reumatoide / Sinoviócitos Limite: Humans Idioma: En Ano de publicação: 2023 Tipo de documento: Article