Cytokine Regulation of Proliferation and ICAM-1 Expression of Human Dermal Microvascular Endothelial Cells In Vitro

Detmar, Michael; Tenorio, Susanne; Hettmannsperger, U.; Ruszczak, Z; Orfanos, Constantin E.

doi:10.1111/1523-1747.ep12555746

Cited by 117 publications

(68 citation statements)

References 44 publications

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“…The exact mechanism by which IL-1Ra exerts this effect is unknown. IL-1 has many pro-angiogenic activities, including increased expression of vascular growth factors (35,36), endothelial mitogenesis (37), and induction of matrix metalloproteinases (36); IL-1Ra presumably can negate all of them. However, our data indicating that IL-1Ra blocks bFGF-and VEGF-induced angiogenesis in the cornea are particularly intriguing in that increasing evidence suggests that these vascular growth factors play a prominent role in the pathogenesis of RA.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of interleukin‐1 but not tumor necrosis factor suppresses neovascularization in rat models of corneal angiogenesis and adjuvant arthritis

Coxon¹,

Bolon²,

Estrada³

et al. 2002

Arthritis & Rheumatism

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Objective. To assess the capacities of the cytokine inhibitors interleukin-1 receptor antagonist (IL-1Ra; anakinra) and PEGylated soluble tumor necrosis factor receptor I (PEG sTNFRI; pegsunercept) to suppress neovascularization.Methods. A corneal angiogenesis assay was performed by implanting nylon discs impregnated with an angiogenic stimulator (basic fibroblast growth factor or vascular endothelial growth factor) into one cornea of female Sprague-Dawley rats. Animals were treated with IL-1Ra or PEG sTNFRI for 7 days, after which new vessels were quantified. In a parallel study, male Lewis rats with mycobacteria-induced adjuvant-induced arthritis were treated with IL-1Ra or PEG sTNFRI for 7 days beginning at disease onset, after which scores for inflammation and bone erosion as well as capillary counts were acquired from sections of arthritic hind paws.Results. Treatment with IL-1Ra yielded a dosedependent reduction in growth factor-induced corneal angiogenesis, while PEG sTNFRI did not. IL-1Ra, but not PEG sTNFRI, significantly reduced the number of capillaries in arthritic paws, even though both anticytokines reduced inflammation and bone erosion to a similar degree.Conclusion. These data support a major role for IL-1, but not TNF␣, in angiogenesis and suggest that an additional antiarthritic mechanism afforded by IL-1 inhibitors, but not anti-TNF agents, is the suppression of the angiogenic component of pannus.

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Section: Discussionmentioning

confidence: 99%

Inhibition of interleukin‐1 but not tumor necrosis factor suppresses neovascularization in rat models of corneal angiogenesis and adjuvant arthritis

Coxon¹,

Bolon²,

Estrada³

et al. 2002

Arthritis & Rheumatism

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“…BK and IL-1 can elicit new blood vessel formation by multiple pathways. IL-1 may have a direct action since it is potent inducer of collagenase (Dinarello, 1991) and a mitogen for microvascular endothelial cells (Detmar et al, 1992). In contrast, it is not known if BK has a direct action in angiogenesis.…”

Section: Discussionmentioning

confidence: 99%

[Leu⁸]des‐Arg⁹‐bradykinin inhibits the angiogenic effect of bradykinin and interleukin‐1 in rats

Fan

1993

British J Pharmacology

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Subcutaneous implantation of sterile polyether sponges in rats elicited a reproducible neovascular response over 14 days, as determined by measurements of relative sponge blood flow by a 133Xe clearance technique. The angiogenic response was verified by quantitation of haemoglobin contents and histological evaluation of vascularized sponges. Daily administration of 1 nmol of bradykinin (BK) into the implants significantly enhanced the basal sponge‐induced neovascularization, leading to higher 133Xe clearance values, increased haemoglobin contents, cellularity and vascularity. When given alone, lower doses of BK (10 pmol) or recombinant human interleukin‐1 α (IL‐1α, 0.3 pmol) produced no apparent effects on the basal sponge‐induced angiogenesis. However, co‐administration of these two peptides produced an angiogenic response similar to that elicited by 1 nmol of BK. The BK/IL‐1α‐induced neovascularization was abolished by the bradykinin B1 receptor antagonist, [Leu8]des‐Arg9‐BK (1 nmol day−1), but not by the B2 receptor antagonist Ac‐d‐Arg‐[Hyp3,d‐Phe7,Leu8]‐BK (1 nmol day−1). Thus, if such interaction between BK and IL‐1α contributes to the excessive neovascularization in chronic inflammatory diseases, the blockade of B1 receptors may provide an effective treatment.

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“…After 72 hours, cells were incubated with 5-methylumbelliferylheptanoate as described. 40 The intensity of fluorescence, proportional to the number of viable cells, was measured using a SpectraMax Gemini EM microplate reader (Bucher Biotec AG).…”

Section: Proliferation Migration Apoptosis Tube Formation and Sprmentioning

confidence: 99%

Growth Hormone Promotes Lymphangiogenesis

Bänziger-Tobler

Halin

Kajiya

et al. 2008

The American Journal of Pathology

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The lymphatic system plays an important role in inflammation and cancer progression, although the molecular mechanisms involved are poorly understood. As determined using comparative transcriptional profiling studies of cultured lymphatic endothelial cells versus blood vascular endothelial cells, growth hormone receptor was expressed at much higher levels in lymphatic endothelial cells than in blood vascular endothelial cells. These findings were confirmed by quantitative real-time reverse transcriptase-polymerase chain reaction and Western blot analyses. Growth hormone induced in vitro proliferation, sprouting, tube formation, and migration of lymphatic endothelial cells, and the mitogenic effect was independent of vascular endothelial growth factor receptor-2 or -3 activation. Growth hormone also inhibited serum starvation-induced lymphatic endothelial cell apoptosis. No major alterations of lymphatic vessels were detected in the normal skin of bovine growth hormone-transgenic mice. However, transgenic delivery of growth hormone accelerated lymphatic vessel ingrowth into the granulation tissue of full-thickness skin wounds, and intradermal delivery of growth hormone resulted in enlargement and enhanced proliferation of cutaneous lymphatic vessels in wild-type mice. These results identify growth hormone as a novel lymphangiogenic factor. (Am J

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Cytokine Regulation of Proliferation and ICAM-1 Expression of Human Dermal Microvascular Endothelial Cells In Vitro

Cited by 117 publications

References 44 publications

Inhibition of interleukin‐1 but not tumor necrosis factor suppresses neovascularization in rat models of corneal angiogenesis and adjuvant arthritis

Inhibition of interleukin‐1 but not tumor necrosis factor suppresses neovascularization in rat models of corneal angiogenesis and adjuvant arthritis

[Leu⁸]des‐Arg⁹‐bradykinin inhibits the angiogenic effect of bradykinin and interleukin‐1 in rats

Growth Hormone Promotes Lymphangiogenesis

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Cytokine Regulation of Proliferation and ICAM-1 Expression of Human Dermal Microvascular Endothelial Cells In Vitro

Cited by 117 publications

References 44 publications

Inhibition of interleukin‐1 but not tumor necrosis factor suppresses neovascularization in rat models of corneal angiogenesis and adjuvant arthritis

Inhibition of interleukin‐1 but not tumor necrosis factor suppresses neovascularization in rat models of corneal angiogenesis and adjuvant arthritis

[Leu8]des‐Arg9‐bradykinin inhibits the angiogenic effect of bradykinin and interleukin‐1 in rats

Growth Hormone Promotes Lymphangiogenesis

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Product

Resources

About

[Leu⁸]des‐Arg⁹‐bradykinin inhibits the angiogenic effect of bradykinin and interleukin‐1 in rats