Gliostatin/platelet-derived endothelial cell growth factor as a clinical marker of rheumatoid arthritis and its regulation in fibroblast-like synoviocytes

Waguri, Y; Otsuka, Takanobu; Sugimura, Isamu; Matsui, Nobuo; Asai, Kiyofumi; Moriyama, Akihiko; Kato, Taiji

doi:10.1093/rheumatology/36.3.315

Cited by 32 publications

(29 citation statements)

References 23 publications

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“…Gliostatin production by FLSs is significantly increased by TNF-a in a dose-dependent manner [14]. The results of the present study demonstrate that TNF-a also induces GLS production in RA FLSs, and the in vitro GLS and MMP-3 production of RA FLSs is down-regulated by FK506 treatment.…”

Section: Discussionsupporting

confidence: 60%

“…Synoviocyte culture and cytotoxicity assay Samples were obtained from the superficial layer of the synovial tissue with active synovitis following our standard protocol [13,14,28]. Tissues were washed with Ca 2?…”

Section: Patientsmentioning

confidence: 99%

“…We previously demonstrated significantly higher concentrations of GLS in the sera and synovial fluids of RA patients compared to those with osteoarthritis or normal controls [11,12]. In addition, the production of GLS by cultured RA fibroblast-like synoviocytes (FLSs) was enhanced by IL-1b [13], TNF-a [14] and GLS itself [15]. We also reported that intraarticular injection of GLS into rabbit knees induced RA-like synovitis [16] and that GLS induced VEGF expression in FLSs [13].…”

Section: Introductionmentioning

confidence: 96%

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FK506 inhibition of gliostatin/thymidine phosphorylase production induced by tumor necrosis factor-α in rheumatoid fibroblast-like synoviocytes

et al. 2010

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Gliostatin/thymidine phosphorylase (GLS/TP) is known to have angiogenic and arthritogenic activities. The purpose of this study was to determine the inhibitory effects of FK506 (tacrolimus) on GLS production in rheumatoid arthritis (RA). We investigated the modulation of serum GLS by FK506 therapy and the effect of FK506 on the production of GLS in fibroblast-like synoviocytes (FLSs). Serum samples were collected from 11 RA patients with active disease at baseline and after 12 weeks of FK506 treatment. Serum concentrations of GLS and matrix metalloproteinase (MMP)-3 were measured by ELISA and found to be down-regulated in responders evaluated with a disease activity score. Patient FLSs were cultured and stimulated by tumor necrosis factor (TNF)-α with or without FK506. The expression levels of GLS were determined using reverse transcription-polymerase chain reaction (RT-PCR) and enzyme immunoassay and shown to be significantly increased. GLS levels in TNF-α-stimulated FLSs were reduced by FK506 treatment. Our data show a novel mechanism for the action of physiological concentrations of FK506 in RA that regulates the production of GLS in FLSs.

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Section: Discussionsupporting

confidence: 60%

Section: Patientsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 96%

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FK506 inhibition of gliostatin/thymidine phosphorylase production induced by tumor necrosis factor-α in rheumatoid fibroblast-like synoviocytes

et al. 2010

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“…We found that GLS is present in high concentrations in synovial¯uids and sera from patients with RA [16] and that its concentration correlates closely with RA disease activity [17]. Gliostatin was detected in synovia of patients with RA [17], and its expression was induced by tumor necrosis factor a (TNF-a), interleukin-1a (IL-1a), IL-6, and IL-8 in cultured human ®broblast-like synoviocytes (FLSs) [18]. Recently we reported that GLS induced MMP-1, MMP-3, and GLS itself in FLSs [19].…”

Section: Introductionmentioning

confidence: 99%

IL-1β-induced expression of matrix metalloproteinases and gliostatin/platelet-derived endothelial cell growth factor (GLS/PD-ECGF) in a chondrosarcoma cell line (OUMS-27)

Ieda

Waguri-Nagaya

Iwahasi

et al. 2001

Rheumatology International

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The purpose of this study was to examine how chondrocytes are involved in the molecular mechanism of inflammation in rheumatoid arthritis (RA). A chondrosarcoma cell line (OUMS-27) was cultured and treated with interleukin-1beta (IL-1beta). Changes in the expression levels of matrix metalloproteinase-1 (MMP-1), metalloproteinase-13 (MMP-13), and gliostatin/platelet-derived endothelial cell growth factor (GLS/PD-ECGF) were assessed by reverse transcription polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assays. IL-1beta induced the expressions of MMP-1, MMP-13, and GLS mRNAs and proteins in a dose-dependent manner. Selective inhibition of the p38 mitogen-activated protein kinase (p38 MAPK) pathway with SB 203580 and SB 202190 blocked the expression of MMP-1, MMP-13, and GLS more strongly than selective in hibition of the extracellular signal-regulated kinase 1 and 2 (ERK1/2) pathway by PD 98059. These findings suggest that chondrocytes may intensify cartilage destruction and inflammation in RA by the induction of MMP-1, MMP-13, and GLS by IL-1beta and that the p38 MAPK pathway plays an important role in these inductions.

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“…In the series of our studies, we detected that the GLS level in synovial¯uid and serum was markedly higher in RA patients than in osteoarthritis patients and normal controls. We aslo found that GLS was produced by ®broblast-like synoviocytes as well as synovial lining cells [16,17], and its production was potentiated by IL-1 and TNF-a [18]. We have already demonstrated the chemical identity of GLS and plateletderived endothelial cell growth factor (PD-ECGF) [19].…”

Section: Introductionmentioning

confidence: 99%

Synovial inflammation and hyperplasia induced by gliostatin/platelet-derived endothelial cell growth factor in rabbit knees

Waguri-Nagaya

Otsuka

Sugimura

et al. 2000

Rheumatology International

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Neovascularization, proliferation of synovial cells, and mononuclear cell influx and activation are characteristic events observed in synovial joints in the pathohistology of rheumatoid arthritis (RA). The objective of this study was to examine synovial inflammation in rabbit knees induced by intra-articular administration of human gliostatin/platelet-derived endothelial cell growth factor (GLS/PD-ECGF), which shares a high degree of chemical homology with thymidine phosphorylase (dThdPase) and is known to have angiogenic activity. Purified recombinant human gliostatin (rHuGLS) and its mutant protein, which was prepared by site-directed mutagenesis and which lacks dThdPase activity, were administered at various doses to rabbit knee joints. The effects of rHuGLS and the mutant were examined histologically. Intra-articular injection of rHuGLS resulted in the development of diffuse synovitis resembling RA. The mutant protein also brought about the same effect. These findings suggest that human GLS can cause RA-like synovitis in rabbit knee joints via a mechanism other than its dThdPase activity.

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Gliostatin/platelet-derived endothelial cell growth factor as a clinical marker of rheumatoid arthritis and its regulation in fibroblast-like synoviocytes

Cited by 32 publications

References 23 publications

FK506 inhibition of gliostatin/thymidine phosphorylase production induced by tumor necrosis factor-α in rheumatoid fibroblast-like synoviocytes

FK506 inhibition of gliostatin/thymidine phosphorylase production induced by tumor necrosis factor-α in rheumatoid fibroblast-like synoviocytes

IL-1β-induced expression of matrix metalloproteinases and gliostatin/platelet-derived endothelial cell growth factor (GLS/PD-ECGF) in a chondrosarcoma cell line (OUMS-27)

Synovial inflammation and hyperplasia induced by gliostatin/platelet-derived endothelial cell growth factor in rabbit knees

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