Specific binding of endocrine transforming growth factor-beta 1 to vascular endothelium.

Dickson, Kathleen M.; Philip, Anie; Warshawsky, H.; O’Connor-McCourt, Maureen D.; Bergeron, John J.M.

doi:10.1172/jci117955

Cited by 35 publications

(18 citation statements)

References 82 publications

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“…The results let us speculate that PC might endocytose LTBP mainly from extrahepatic sources as a result of clearance functions of the liver for circulating latent TGF-␤. A role of this cell type in the catabolism of bloodborne TGF-␤ has been proposed previously, 52,53 but it is presently not known whether this cytokine circulates in the blood as a component of the large, latent complex, or only bound to ␣ 2 -macroglobulin. [54][55][56] PC, however, could also be relevant for the sequestration of locally produced TGF-␤ complex.…”

Section: Discussionmentioning

confidence: 97%

Expression and Matrix Deposition of Latent Transforming Growth Factor β Binding Proteins in Normal and Fibrotic Rat Liver and Transdifferentiating Hepatic Stellate Cells in Culture

et al. 2001

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Section: Discussionmentioning

confidence: 97%

Expression and Matrix Deposition of Latent Transforming Growth Factor β Binding Proteins in Normal and Fibrotic Rat Liver and Transdifferentiating Hepatic Stellate Cells in Culture

et al. 2001

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“…Additionally, PDGF-BB also induces the differentiation of undifferentiated mesenchymal cells towards a mural cell fate (Hellstrom et al, 1999;Hirschi et al, 1999). In addition, transforming growth factor beta (TGF-β)-mediated signalling pathways play an important role in the interaction between mural cells/pericytes and endothelial cells (Dickson et al, 1995). TGF-β acts in a pleiotropic manner and dose-dependently on the angiogenic process.…”

Section: Discussionmentioning

confidence: 99%

Comparative study assessing effects of sonic hedgehog and VEGF in a human co-culture model for bone vascularisation strategies

Dohle

Fuchs²,

Kolbe³

et al. 2011

eCM

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“…TGFP has specific binding sites on endothelium (38). It is able to trigger angiogenesis (14), but can also inhibit endothelial cell adhesiveness for neutrophils in vitro (39) and in vivo (40), possibly through the reduced expression of E-selectin, which is an adhesion molecule present on endothelial cells (41).…”

Section: Discussionmentioning

confidence: 99%

Inhibition and prevention of monosodium urate monohydrate crystal–induced acute inflammation in vivo by transforming growth factor β1

Lioté

Prudhommeaux

Schiltz

et al. 1996

Arthritis & Rheumatism

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Objective. We investigated the effects of transforming growth factor Pl (TGFP1) on monosodium urate monohydrate (MSU) crystal-induced acute inflammation in vivo.Methods. One hour after MSU crystal-induced acute inflammation was produced in the rat subcutaneous air pouch model, the effects of recombinant human TGFPl (rHuTGFP1; 10-100 pglanimal) and ultrapure TGFPl (UPTGFPI; 100 and 500 pglanimal) were assessed, based on absolute and differential white blood cell counts in the exudate. The effects of 10 pg of rHuTGFP1 preincubated with a specific anti-TGFP antibody, and the effects of coinjection of crystals and rHuTGFP1, were also studied.Results. UPTGFPl and rHuTGFPl markedly reduced MSU crystal-induced inflammation. Recombinant human TGFPl also reduced inflammation when administered concomitantly with MSU crystals. Moreover, rHuTGFPl and UPTGFP1, injected l hour after MSU crystal injection, reduced the inflammatory response in a dose-dependent manner. Injection of rHuTGFPl (100 pglanimal) resulted in a >9w0 reduction in the maximal white blood cell count, achieved 6 hours after Spontaneous resolution is an important clinical feature of gouty attacks that is not yet fully understood (1,2). Lowering of pH and stimulation of phagocyte oxidative metabolism during crystal-induced inflammation may promote monosodium urate monohydrate (MSU) crystal dissolution. However, this cannot entirely explain the self-limited nature of gouty inflammation, since MSU crystals can remain in the synovial fluid after acute inflammation and have been identified in noninflammatory synovial fluids from gout patients (3).In vitro (4) and in vivo ( 5 ) studies have shown that changes in the protein coating of MSU crystals and in other as-yet-unidentified components that are generated locally during subsiding inflammation probably contribute to the self-limited nature of acute gouty arthritis (6). There is strong in vitro evidence that proinflammatory cytokines such as interleukin-lP (ILlP), tumor necrosis factor P (TNFP), IL-6, and IL-8 (7-1 1) are released within hours when monocytes and macrophages are incubated with MSU crystals. Natural cytokine inhibitors such as IL-1 receptor antagonist (IL-1Ra) and/or soluble TNFa receptor, or other regulatory cytokines such as IL-4 and IL-10, may block acute and subsequent chronic inflammation.

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Specific binding of endocrine transforming growth factor-beta 1 to vascular endothelium.

Cited by 35 publications

References 82 publications

Expression and Matrix Deposition of Latent Transforming Growth Factor β Binding Proteins in Normal and Fibrotic Rat Liver and Transdifferentiating Hepatic Stellate Cells in Culture

Expression and Matrix Deposition of Latent Transforming Growth Factor β Binding Proteins in Normal and Fibrotic Rat Liver and Transdifferentiating Hepatic Stellate Cells in Culture

Comparative study assessing effects of sonic hedgehog and VEGF in a human co-culture model for bone vascularisation strategies

Inhibition and prevention of monosodium urate monohydrate crystal–induced acute inflammation in vivo by transforming growth factor β1

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