Induction of IL-8, MCP-1, and bFGF by TNF-α in retinal glial cells: implications for retinal neovascularization during post-ischemic inflammation

Yoshida, Shigeo; Yoshida, Ayako; Ishibashi, Tatsuro

doi:10.1007/s00417-004-0874-2

Cited by 128 publications

(85 citation statements)

References 18 publications

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“…TNF-is an angiogenic molecule produced by hypoxic monocytes/macrophages (Yun, et al, 1997) and is a likely mediator of retinal neovascularization/revascularization. It has been reported that TNF-level is higher in patients with PDR (Limb, et al, 2001), and we have detected this molecule in the macrophages/BM-MLCs in murine OIR (Yoshida, et al, 2004). Moreover, we have demonstrated that TNF-up-reguletes the production of IL-8, VEGF, bFGF, or MCP-1 in retinal vascular cells and/or glial cells adjacent to microvessels triggering neovascularization/revascularization in an autocrine or paracrine manner (Yoshida, et al, 2004;Yoshida, et al, 1997).…”

supporting

confidence: 69%

“…It has been reported that TNF-level is higher in patients with PDR (Limb, et al, 2001), and we have detected this molecule in the macrophages/BM-MLCs in murine OIR (Yoshida, et al, 2004). Moreover, we have demonstrated that TNF-up-reguletes the production of IL-8, VEGF, bFGF, or MCP-1 in retinal vascular cells and/or glial cells adjacent to microvessels triggering neovascularization/revascularization in an autocrine or paracrine manner (Yoshida, et al, 2004;Yoshida, et al, 1997). These processes are likely to be important in promoting macrophages/ BM-MLCs-related retinal neovascularization/revascularization in hypoxic retinas.…”

supporting

confidence: 69%

See 1 more Smart Citation

Fibrovascular Membranes Associated with PDR: Development of Molecular Targets by Global Gene Expression Profiling

Ishikawa¹,

Arima²,

Asato³

et al. 2012

Diabetic Retinopathy

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supporting

confidence: 69%

supporting

confidence: 69%

Fibrovascular Membranes Associated with PDR: Development of Molecular Targets by Global Gene Expression Profiling

Ishikawa¹,

Arima²,

Asato³

et al. 2012

Diabetic Retinopathy

Self Cite

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“…The VEGF through VEGFR2 induces endothelial cell proliferation and increases cerebral vascular permeability, whereas interaction of Ang-1 with its receptor, Tie2, protects against VEGFinduced brain-blood barrier leakage (Thurston et al, 1999(Thurston et al, , 2000Wu et al, 2003). The TNF/TNFR1 can directly act on endothelial cells to induce angiogenesis through activation of the VEGF pathway (Sugano et al, 2004;Yoshida et al, 2004). Our data showed that both rhTNF and rhEPO, but not rhTNF or rhEPO alone, at the concentration used in this study upregulated VEGF/VEGFR2 and Ang1/ Tie2, which was mediated by EPOR.…”

Section: Figurementioning

confidence: 99%

Tumor Necrosis Factor α Primes Cerebral Endothelial Cells for Erythropoietin-Induced Angiogenesis

Wang

Chopp

Hua³

et al. 2010

J Cereb Blood Flow Metab

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Erythropoietin (EPO) enhances angiogenesis in the ischemic brain. Stroke induces secretion of tumor necrosis factor a (TNF-a). We investigated the effect of TNF-a on EPO-induced in vitro angiogenesis in cerebral endothelial cells. Using a capillary-like tubular formation assay, we found that transient incubation of primary rat cerebral microvascular endothelial cells (RECs) with TNF-a substantially upregulated EPO receptor (EPOR) expression and addition of EPO into TNF-a-treated RECs significantly augmented the capillary-like tube formation. Blockage of TNF receptor 1 (TNFR1) suppressed TNF-a-upregulated EPOR expression and abolished EPO-induced tube formation. Attenuation of endogenous EPOR with small interfering RNA (siRNA) also inhibited EPO-enhanced tube formation. Treatment of RECs with EPO activated nuclear factor-kappa B (NF-jB) and Akt. Incubation of the TNF-a-treated endothelial cells with EPO activated vascular endothelial growth factor (VEGF), VEGF receptor 2 (VEGFR2), angiopoietin 1 (Ang1), and Tie2. Blockage of VEGFR2 and Tie2 resulted in reduction of EPO-augmented tube formation. These data indicate that interaction of TNF-a with TNFR1 sensitizes cerebral endothelial cells for EPO-induced angiogenesis by upregulation of EPOR, which amplifies the effect of EPO on activation of the VEGF/VEGFR2 and Ang1/Tie2 pathways. Our results provide the evidence for crosslink between TNF and EPOR to coordinate the onset of angiogenesis in cerebral endothelial cells.

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“…Moreover, previous reports have shown that retinal ischaemia stimulates IL-8 and MCP-1 production, and both chemokines are involved in retinal neovascularization. [31][32][33][34] Although ischaemia as seen using FFA was one of the exclusion criteria, we cannot absolutely exclude that this was present in our patients. So retinal ischaemia may have also contributed to hyperproduction of IL-8 and MCP-1.…”

Section: Il-8 and Mcp-1 In Brvo Macular Oedemamentioning

confidence: 99%

Vitreous levels of interleukine-8 and monocyte chemoattractant protein-1 in macular oedema with branch retinal vein occlusion

Fonollosa¹,

García-Arumí

Santos

et al. 2010

Eye

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Purpose To investigate whether interleukine-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) are related with macular oedema in patients with branch retinal vein occlusions (BRVOs). Design Retrospective case-control study. Participants Nineteen patients who had macular oedema due to BRVO and nine patients with non-ischaemic ocular diseases (control group). Methods Macular oedema was examined by optical coherence tomography. Both venous blood and vitreous samples were obtained at the time of vitreoretinal surgery. IL-8 and MCP-1 levels in vitreous fluid and plasma were determined with enzyme-linked immunosorbent assay kits. Variables were compared with the Mann-Whitney U-test, Wilcoxon's signed-ranked test, and the v 2 -test, when appropriate. To examine correlations, Spearman's rank-order correlation coefficients were calculated. Statistical significance was set at Po0.05. Results The vitreous fluid levels of IL-8 (median: 63.5 pg/ml) and MCP-1 (median: 1522.4 pg/ml) were significantly higher in the patients with BRVO than in the control group (median: 5.1 and 746.5 pg/ml respectively; Po0.001 and o0.001 respectively). Vitreous IL-8 and MCP-1 were significantly correlated in patients with BRVO (P ¼ 0.009). Conclusions Both IL-8 and MCP-1 were elevated in the vitreous fluid of patients with BRVO and macular oedema. Both chemokines may contribute to the pathogenesis of macular oedema in patients with BRVO.

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Induction of IL-8, MCP-1, and bFGF by TNF-α in retinal glial cells: implications for retinal neovascularization during post-ischemic inflammation

Abstract: The results indicate that TNF-alpha is produced by activated macrophages/microglia and may participate in retinal neovascularization during post-ischemic inflammation through the induction of potent angiogenic factors in an autocrine or paracrine manner.

Cited by 128 publications

References 18 publications

Fibrovascular Membranes Associated with PDR: Development of Molecular Targets by Global Gene Expression Profiling

Fibrovascular Membranes Associated with PDR: Development of Molecular Targets by Global Gene Expression Profiling

Tumor Necrosis Factor α Primes Cerebral Endothelial Cells for Erythropoietin-Induced Angiogenesis

Vitreous levels of interleukine-8 and monocyte chemoattractant protein-1 in macular oedema with branch retinal vein occlusion

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