OBJECTIVES: to evaluate the rheumatoid synovial cell capacity to produce superoxide anion in response to interleukin-1beta (IL-1beta) and tumour necrosis factor-alpha (TNF-alpha), and to study the NADPH oxidase involvement in this production. MATERIAL AND METHODS: Synovial cells obtained from 7 rheumatoid arthritis (RA), 5 osteoarthritic (OA) patients, and dermal fibroblasts, were stimulated (i) with IL-1beta and TNF-alpha, or (ii) with specific oxidase activators and inhibitors, before studying superoxide production; we also studied NADPH oxidase mRNAs and protein expression, and p47-phox phosphorylation. RESULTS: Constitutive superoxide production by RA cells was increased in comparison to OA cells and dermal fibroblasts, and was stimulated by PMA and ionomycin. This production was increased after cytokine treatment of RA synovial cells. Cytokine-induced superoxide production by RA cells was inhibited by iodonium diphenyl or apocynin, suggesting the involvement of NADPH oxidase. RT-PCR and western blot analysis revealed the presence of p47-phox, gp91-phox and Nox4 in RA and OA cells, and in dermal fibroblasts. P47-phox phosphorylation was enhanced after cytokine-treatment in RA and OA cells, suggesting a PKC-mediated up-regulation of NADPH oxidase. CONCLUSIONS: NADPH oxidase is involved in the superoxide release by RA synovial cells, constitutively and after cytokine up-regulation. These cells express two different homologues (gp91-phox and Nox4).
OBJECTIVES: to evaluate the rheumatoid synovial cell capacity to produce superoxide anion in response to interleukin-1beta (IL-1beta) and tumour necrosis factor-alpha (TNF-alpha), and to study the NADPH oxidase involvement in this production. MATERIAL AND METHODS: Synovial cells obtained from 7 rheumatoid arthritis (RA), 5 osteoarthritic (OA) patients, and dermal fibroblasts, were stimulated (i) with IL-1beta and TNF-alpha, or (ii) with specific oxidase activators and inhibitors, before studying superoxide production; we also studied NADPH oxidase mRNAs and protein expression, and p47-phox phosphorylation. RESULTS: Constitutive superoxide production by RA cells was increased in comparison to OA cells and dermal fibroblasts, and was stimulated by PMA and ionomycin. This production was increased after cytokine treatment of RA synovial cells. Cytokine-induced superoxide production by RA cells was inhibited by iodonium diphenyl or apocynin, suggesting the involvement of NADPH oxidase. RT-PCR and western blot analysis revealed the presence of p47-phox, gp91-phox and Nox4 in RA and OA cells, and in dermal fibroblasts. P47-phox phosphorylation was enhanced after cytokine-treatment in RA and OA cells, suggesting a PKC-mediated up-regulation of NADPH oxidase. CONCLUSIONS: NADPH oxidase is involved in the superoxide release by RA synovial cells, constitutively and after cytokine up-regulation. These cells express two different homologues (gp91-phox and Nox4).
Authors: Yessica Zamudio-Cuevas; Cristina Hernández-Díaz; Carlos Pineda; Anthony M Reginato; Jorge Francisco Cerna-Cortés; Lucio Ventura-Ríos; Alberto López-Reyes Journal: Clin Rheumatol Date: 2015-04-09 Impact factor: 2.980
Authors: Dong Hoon Yu; Jun Koo Yi; Hyung Soo Yuh; Seo jin Park; Hei Jung Kim; Ki Beom Bae; Young Rae Ji; Na Ri Kim; Si Jun Park; Do Hyung Kim; Sung Hyun Kim; Myoung Ok Kim; Jeong Woong Lee; Zae Young Ryoo Journal: Exp Mol Med Date: 2012-09-30 Impact factor: 8.718
Authors: Yessica Zamudio-Cuevas; Karina Martínez-Flores; Javier Fernández-Torres; Yahir A Loissell-Baltazar; Daniel Medina-Luna; Ambar López-Macay; Javier Camacho-Galindo; Cristina Hernández-Díaz; Mónica G Santamaría-Olmedo; Edgar Oliver López-Villegas; Francesca Oliviero; Anna Scanu; Jorge Francisco Cerna-Cortés; Marwin Gutierrez; Carlos Pineda; Alberto López-Reyes Journal: Arthritis Res Ther Date: 2016-05-21 Impact factor: 5.156