Effect of interleukin-4 on vascular endothelial growth factor production in rheumatoid synovial fibroblasts

Hong, Ki Hwan; Cho, M. L.; Min, Sung−Wook; Shin, Yu-Ju; Yoo, Sehoon; Choi, Jin; Kim, Wan‐Uk; Song, Seok-Whan; Cho, C. S.

doi:10.1111/j.1365-2249.2006.03295.x

Cited by 39 publications

(42 citation statements)

References 46 publications

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“…These cytokines inhibit the release of VEGF and other angiogenic mediators [5,6,12,70,87]. For example, IL-4 blocks VEGF release by RA synovial fibroblasts [87]. IL-4 and IL-13 gene transfer inhibited synovial inflammation and angiogenesis in rats [88,89] (Table II).…”

Section: Angiogenesis Inhibitors and Their Use In Arthritis Therapymentioning

confidence: 99%

Angiogenesis in rheumatoid arthritis

et al. 2009

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Angiogenesis is the formation of new capillaries from pre-existing vessels. A number of soluble and cell-bound factors may stimulate neovascularization. The perpetuation of angiogenesis involving numerous soluble and cell surface-bound mediators has been associated with rheumatoid arthritis (RA). These angiogenic mediators, among others, include growth factors, primarily vascular endothelial growth factor (VEGF) and hypoxia-inducible factors (HIFs), as well as pro-inflammatory cytokines, various chemokines, matrix components, cell adhesion molecules, proteases and others. Among the several potential angiogenesis inhibitors, targeting of VEGF, HIF-1, angiogenic chemokines, tumor necrosis factor-α and the α V β 3 integrin may attenuate the action of angiogenic mediators and thus synovial angiogenesis. In addition, some naturally produced or synthetic compounds including angiostatin, endostatin, paclitaxel, fumagillin analogues, 2-methoxyestradiol and thalidomide may be included in the management of RA.

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Section: Angiogenesis Inhibitors and Their Use In Arthritis Therapymentioning

confidence: 99%

Angiogenesis in rheumatoid arthritis

et al. 2009

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“…These cytokines inhibit the release of angiogenic mediators and thus they indirectly block neovascularization [2,3,6]. For example, IL-4 suppresses VEGF production by synovial fibroblasts [36]. …”

Section: Angiogenesis: Mechanisms and Clinical Relevancesmentioning

confidence: 99%

New insights in synovial angiogenesis

et al. 2010

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Angiogenesis is the formation of new capillaries from pre-existing vessels. A number of soluble and cell-bound factors may stimulate neovascularization. The perpetuation of angiogenesis involving numerous soluble and cell surface-bound mediators has been associated with rheumatoid arthritis (RA). These angiogenic mediators, among others, include growth factors, primarily vascular endothelial growth factor (VEGF) and hypoxia-inducible factors (HIFs), as well as pro-inflammatory cytokines, various chemokines, cell adhesion molecules, proteases and others. Among the several potential angiogenesis inhibitors, targeting of VEGF, HIF-1, angiopoietin and the α V β 3 integrin, as well as some endogenous or synthetic compounds including angiostatin, endostatin, paclitaxel, fumagillin analogues, 2-methoxyestradiol and thalidomide seems to be promising for the management of synovial inflammation and angiogenesis. A complete review of antiangiogenic drugs used in animal models of arthritis or human RA is available in a table.

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“…ИЛ 4 индуцирует экспрессию молекул MHC II класса на макрофа-гах и дендритных клетках, принимая участие в созревании и активации последних. Важно отметить, что этот цитокин способен подавлять пролиферацию синовиоцитов [51,141,142]. Попытки применения ИЛ 4 при РА с терапевтической целью, в том числе для снижения костной резорбции, не да-ли ожидаемых результатов, несмотря на обнадеживающие данные экспериментов in vivo.…”

Section: ц и т о к и н ы с е к р е т и р у е м ы е T H 1 -и T H 2 -unclassified