Aberrant production of gliostatin/platelet‐derived endothelial cell growth factor in rheumatoid synovium

Takeuchi, Masanori; Otsuka, Takanobu; Matsui, Nobuo; Asai, Kiyofumi; Hirano, Takayoshi; Moriyama, Akihiko; Isobe, Ichiro; Ekşioğlu, Yaman Z.; Matsukawa, Kohei; Kato, Taiji; Tada, Toyohiro

doi:10.1002/art.1780370509

Cited by 50 publications

(35 citation statements)

References 24 publications

(8 reference statements)

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“…How inflammatory cell infiltration leads to microvessel proliferation remains to be elucidated. Although various angiogenic factors, such as bFGF, PDGF, and IL-1 have been shown to support the process of neovascularization [18], no one factor has provided a conclusive explanation for the angiogenesis found in kidney with CTI.…”

Section: Discussionmentioning

confidence: 99%

“…Because TP is identical to PD-ECGF, which is a chemotactic and angiogenic factor for endothelial cells [10, 11], TP and its degradation product, 2-deoxy- D -ribose, are recognized as endothelial-cell chemoattractants and angiogenesis-inducing factors [9,10,11,12,13,14]. Inflammatory cells, such as macrophages, express TP in inflammatory diseases [13,17,18,19,20], as do infiltrating macrophages in a variety of tumors [9, 12, 21, 22]. …”

Section: Discussionmentioning

confidence: 99%

“…Inflammatory cells such as macrophages express TP in inflammatory diseases [13,17,18,19,20], as do infiltrating macrophages in a variety of tumors [8, 12, 21, 22]. Activated macrophages are a major component of chronic inflammation and play a key role in progressive interstitial injury [23, 24].…”

Section: Introductionmentioning

confidence: 99%

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Upregulation of Thymidine Phosphorylase in Chronic Glomerulonephritis and Its Role in Tubulointerstitial Injury

Wang¹,

Goh²,

Moon³

et al. 2005

Nephron Clin Pract

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Chronic tubulointerstitial injury (CTI), commonly a sequel to chronic glomerulonephritis (CGN), is associated with the proliferation of new blood vessels. Angiogenesis is an essential process in chronic inflammation, and is controlled by a number of angiogenic factors including thymidine phosphorylase (TP). Knowledge of TP in renal disease is still rudimentary, and its role in CGN has not been explored. We analyzed the expression of TP by RTPCR, immunohistology and in situ hybridization in 20 human kidneys with CGN. To evaluate the degree of angiogenesis, we counted the microvessel density (MVD). MVD was significantly higher in all categories of CGN, between 19.7 ± 7.7 and 58.9 ± 7.5, compared to control value, 12.7 ± 5.0 (p< 0.05). MVD was increased in areas of abundant mononuclear cell infiltration with minimal interstitial fibrosis, and decreased or absent in areas of marked fibrosis. There was a significant correlation between MVD and interstitial fibrosis (p < 0.0001). TP mRNA was upregulated for all categories of CGN. TP was strongly expressed by mononuclear inflammatory cells and in most atrophic tubules. Each MVD and interstitial volume was significantly correlated with both the number of TP+ mononuclear cells and TP+ tubular cells, respectively (p < 0.0001). We have demonstrated an upregulation of TP and increase in MVD in areas of CTI in a variety of CGN. The up-regulation of TP may contribute to angiogenesis, which may play a critical role in the progression of interstitial fibrosis in CGN.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Upregulation of Thymidine Phosphorylase in Chronic Glomerulonephritis and Its Role in Tubulointerstitial Injury

Wang¹,

Goh²,

Moon³

et al. 2005

Nephron Clin Pract

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“…Over-expression of TPase has also been implicated in inflammatory disease states including rheumatoid arthritis and psoriasis 124,125 . TPase catalyzes the reversible phosphorolysis of thymidine to thymine and 2-deoxyribose 1-phosphate 126 .…”

Section: Thymidine Phosphorylasementioning

confidence: 99%

Multisubstrate adduct inhibitors: Drug design and biological tools

Calvez

Scott²,

Migaud

2009

Journal of Enzyme Inhibition and Medicinal Chemistry

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“…Elevated levels of TP expression have also been associated with the pathophysiology of other inflammatory diseases, including: 1) rheumatoid arthritis, where TP was found to be highly elevated in synovial fluid and where there was an increase in TP mRNA in cultured rheumatoid arthritis fibroblast-like synoviocytes; 2) psoriasis, where there was an increase in TP expression in psoriatic lesions, including increased TP mRNA in lesional epidermis and increased TP expression in basal keratinocytes and suprabasal layers; and 3) gastric ulcers, in which TP was elevated near gastric ulcer margins compared with uninvolved fundic and pyloric stomach (Takeuchi et al, 1994;Creamer et al, 1997;Kusugai et al, 1997;Muro et al, 1999). Plasma TP was found to be higher in intractable gastric ulcer patients compared with either healthy persons, patients with duodenal ulcers, or patients with gastric ulcer with significant resolution (Kusugai et al, 1997).…”

mentioning

confidence: 99%

Expression of the Angiogenic Factor Thymidine Phosphorylase in THP-1 Monocytes: Induction by Autocrine Tumor Necrosis Factor-α and Inhibition by Aspirin

Zhu

Schwartz²

2003

Mol Pharmacol

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The angiogenic factor thymidine phosphorylase (TP) is highly expressed in human monocytes and macrophages, and its expression has been linked to the pathology and progression of solid tumors, rheumatoid arthritis, and gastric ulcers. In this study, TP mRNA and enzyme activity were found to be upregulated upon the induction of differentiation of the human monocyte cell line THP-1 by phorbol 12-myristate 13-acetate (PMA). TP expression in THP-1 cells was similarly increased by tumor necrosis factor-␣ (TNF␣). Because monocytes and macrophages are a predominant source of TNF␣, the up-regulation of TP upon THP-1 differentiation could have been caused by the autocrine production of TNF␣. In support of this hypothesis, PMA increased TNF␣ mRNA levels; furthermore, the increase in TP expression with PMA treatment was partially blocked by a neutralizing antibody to TNF␣, particularly at the earlier time points. This data also suggested there may be additional mechanisms regulating TP expression upon PMA treatment of the cells. The induction of TP by TNF␣ was mimicked by an antibody to the TNF␣ receptor R2 (TNF-R2; p75), but not by an antibody to TNF-R1 (p55), suggesting that the TNF-R2 plays a role in the regulation of TP expression. The PMA-induced increase in TP expression was blocked by aspirin but not by the related agent indomethacin, suggesting that aspirin's effect was not caused by the inhibition of cellular cyclooxygenases. An alternative mechanism by which aspirin inhibits gene expression is the modulation of the transcription factor NFB, and the TNF␣-induced increase in TP mRNA was blocked by a cell-permeable NFB inhibitory peptide. Furthermore, TNF␣ increased and aspirin (but not indomethacin) decreased NFB DNA-binding activity in THP-1 cells. In conclusion, the modulation of TP expression in monocytes by pro-and anti-inflammatory agents suggests that its angiogenic-related actions could contribute to the inflammatory response associated with a number of pathophysiological conditions.

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Aberrant production of gliostatin/platelet‐derived endothelial cell growth factor in rheumatoid synovium

Cited by 50 publications

References 24 publications

Upregulation of Thymidine Phosphorylase in Chronic Glomerulonephritis and Its Role in Tubulointerstitial Injury

Upregulation of Thymidine Phosphorylase in Chronic Glomerulonephritis and Its Role in Tubulointerstitial Injury

Multisubstrate adduct inhibitors: Drug design and biological tools

Expression of the Angiogenic Factor Thymidine Phosphorylase in THP-1 Monocytes: Induction by Autocrine Tumor Necrosis Factor-α and Inhibition by Aspirin

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