Interleukin‐1β induces interleukin‐6 mRNA expression and protein production in synovial cells from human temporomandibular joint

Ogura, Naomi; Tobe, Makiko; Sakamaki, Hiroyuki; Kujiraoka, Hiroaki; Akiba, Masakazu; Abiko, Yoshimitsu; Nagura, Hideaki

doi:10.1034/j.1600-0714.2002.310606.x

Cited by 34 publications

(35 citation statements)

References 36 publications

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“…We also investigated the effects of stimulation of proinflammatory cytokines such as IL-1 and/or TNF-on the gene expression and production of CSFs in synovial fibroblasts from TMJ patients. Human synovial fibroblasts were isolated from the synovial tissues of these patients using the out-growth method of Ogura et al (20). The culture medium used was Table 2 lists the primer sequences used for this analysis.…”

Section: Introductionmentioning

confidence: 99%

<b>Interleukin-1β and Tumor Necrosis Factor-α Synergistically Induce Expression of Colony Stimulating Factors in Synovial Fibroblasts from the Human Temporomandibular Joint</b>

et al. 2017

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IL-1 and TNF-are proinflammatory cytokines that affect inflammatory responses and matrix degradation. Although interleukin-1 (IL-1 )and tumor necrosis factor-(TNF-) have been detected in the synovial fluids from patients such as temporomandibular joint disorders(TMD), there is little known about the molecular mechanisms of inflammatory conditions of TMD. To identify putative factors associated with temporomandibular joint (TMJ) inflammation, we investigated IL-1 and/or TNF--responsive genes of synovial fibroblasts from patients with TMD using microarray analysis. Granulocyte macrophage colony stimulating factor(GM-CSF)was one of the genes whose expression was strongly up-regulated in synovial fibroblasts by IL-1 and/or TNF-. The gene expressions of macrophage colony stimulating factor(M-CSF)and Granulocyte colony stimulating factor (G-CSF) were also up-regulated by IL-1 and/or TNF-. Gene expression and protein production of GM-CSF and G-CSF, but not of M-CSF, were synergistically increased in synovial fibroblasts stimulated with IL-1 and TNF-. M-CSF protein was only detected in the conditioned medium of the non-stimulated control in which GM-CSF and G-CSF were not detected. In addition, MAPK and NF B inhibitors inhibited IL-1 and TNF-stimulated production of GM-CSF and M-CSF. CSFs act on hemopoietic cells as growth factors and activation/differentiation factors. These results suggest that expression of CSFs in synovial fibroblasts stimulated by IL-1 and/or TNF-is one factor associated with inflammatory progression of the intracapsular pathological conditions of the TMJ.

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Section: Introductionmentioning

confidence: 99%

<b>Interleukin-1β and Tumor Necrosis Factor-α Synergistically Induce Expression of Colony Stimulating Factors in Synovial Fibroblasts from the Human Temporomandibular Joint</b>

et al. 2017

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“…In order to identify the putative factors associated with the intracapsular pathologic condition, we investigated interleukin (IL)-1␤-and/or tumor necrosis factor (TNF)-␣-responsive genes of synoviocytes from patients with ID and/or OA of TMJ [19][20][21][22][23][24][25][26]. According to microarray analysis, a large number of IL-1␤-and/or TNF-␣-responsive genes of synoviocytes were detected [19][20][21].…”

Section: Introductionmentioning

confidence: 99%

Molecular aspects in inflammatory events of temporomandibular joint: Microarray-based identification of mediators

Ogura

Kondoh

2015

Japanese Dental Science Review

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Synovial inflammation (synovitis) frequently accompanies intracapsular pathologic conditions of the temporomandibular joint (TMJ) such as internal derangement (ID) and/or osteoarthritis (OA), and is suggested to be associated with symptom severity. To identify the putative factors associated with synovitis, we investigated interleukin (IL)-1␤-and/or tumor necrosis factor (TNF)-␣-responsive genes of fibroblast-like synoviocytes (FLS) from patients with ID and/or OA of TMJ using microarray analysis. In this review, we first summarize the FLS of TMJ and the signaling pathways of IL-1␤ and TNF-␣. Next, we show the up-regulated genes in FLS after stimulation with IL-1␤ or TNF-␣, and summarize the gene functions based on recent studies. Among the top 10 up-regulated factors, molecules such as IL-6 and cycrooxygense-2 have been well characterized and investigated in the inflammatory responses and tissue destruction associated with joint diseases such as RA and OA, but the roles of some molecules remain unclear. The FLS reaction can lead to the synthesis and release of a wide variety of inflammatory mediators. Some of these mediators are detected in joint tissues and synovial fluids under intracapsular pathologic conditions, and may represent potential targets for therapeutic interventions in ID and/or OA of TMJ.

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“…SFs extracted from rat TMJs were prepared according to the method described in the literature, with minor modifications (Ogura et al, 2002). Briefly, the double condyles of 3-month-old Sprague Dawley rats (~200 g, obtained from the Zhejiang Center of Laboratory Animals, China) were excised.…”

Section: Cell Culturementioning

confidence: 99%

Involvement of the MAPK pathway in the pressure-induced synovial metaplasia procedure for the temporomandibular joint

et al. 2016

Genet. Mol. Res.

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ABSTRACT. Abnormal pressure is an important factor that contributes to bone adaptation in the temporomandibular joint (TMJ). We determined the effect of the mitogen-activated protein kinases (MAPK) pathway on the pressure-induced synovial metaplasia procedure for the TMJ, both in vitro and in vivo. Synovial fibroblasts (SFs) were exacted from rat TMJs and exposed to different hydrostatic pressures. The protein extracts were analyzed to determine the activation of ERK1/2, JNK, and p38. Surgical anterior disc displacement (ADD) was also performed on Japanese rabbits, and the proteins of TMJ were isolated to analyze pressure-induced MAPK activation after 1, 2, 4, and 8 weeks. The results showed that the activation of ERK1/2 and JNK in SFs significantly changed with increasing hydrostatic pressure, whereas p38 activation did not change. Moreover, p38 was activated in animals 1 week after surgical ADD. The levels of p38 gradually increased after 2 and 4 weeks, and then slightly decreased but remained higher than in the control 8 weeks after surgical ADD. Nevertheless, JNK was rarely activated after the ADD treatment. Our findings suggest the involvement of MAPK activation in the pressure-induced synovial metaplasia procedure with pressure loading in TMJ.

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Interleukin‐1β induces interleukin‐6 mRNA expression and protein production in synovial cells from human temporomandibular joint

Abstract: IL-1 beta increased IL-6 production in synovial cells resulting from an increase in IL-6 mRNA expression. Enhanced production of IL-6, which is associated with bone resorption and inflammatory response, seems to be related to the progression of TMJ disorders.

Cited by 34 publications

References 36 publications

<b>Interleukin-1β and Tumor Necrosis Factor-α Synergistically Induce Expression of Colony Stimulating Factors in Synovial Fibroblasts from the Human Temporomandibular Joint</b>

<b>Interleukin-1β and Tumor Necrosis Factor-α Synergistically Induce Expression of Colony Stimulating Factors in Synovial Fibroblasts from the Human Temporomandibular Joint</b>

Molecular aspects in inflammatory events of temporomandibular joint: Microarray-based identification of mediators

Involvement of the MAPK pathway in the pressure-induced synovial metaplasia procedure for the temporomandibular joint

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