Matrix GLA Protein Stimulates VEGF Expression through Increased Transforming Growth Factor-β1 Activity in Endothelial Cells

Boström, Kristina I.; Zebboudj, Amina F.; Yao, Yucheng; Lin, Than S.; Torres, Alejandra

doi:10.1074/jbc.m406868200

Cited by 105 publications

(130 citation statements)

References 62 publications

(83 reference statements)

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“…Others have shown that MGP promotes the growth of BAECs, and that when MGP is present, these cells form enclosures, the basis of the endothelial tube-formation assay (Kubota et al, 1988;Bostrom et al, 2004). We treated BAECs with media conditioned by GBM- ID4 elevates MGP promoting GBM growth PM Kuzontkoski et al derived cell cultures expressing elevated levels of ID4 and found that this media could enhance endothelial cell growth and tube formation (Figure 3).…”

Section: Id4 Elevates Mgp Promoting Gbm Growthmentioning

confidence: 96%

“…To investigate this possibility, we prepared conditioned media from cell cultures expressing different levels of ID4 and observed its effect on the migration and growth of bovine aortic endothelial cells (BAECs) and their ability to form enclosures in a collagen-I tube-formation assay, an in vitro correlate for angiogenesis (Kubota et al, 1988;Bostrom et al, 2004).…”

Section: Id4 Facilitates Growth Of Gbm Xenograftsmentioning

confidence: 99%

“…The expression of 12 genes increased at least twofold and the expression of 26 genes decreased at least twofold when ID4 was elevated (Supplementary Table S1). We systematically searched the literature for information about each of these genes, but the expression patterns and documented biologies associated with these genes did not suggest a function in angiogenesis, except in the case of matrix GLA protein (MGP) (St Croix et al, 2000;Bostrom et al, 2004).…”

Section: Identification Of a Potential Id4 Target Promoting Angiogenementioning

confidence: 99%

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Inhibitor of DNA binding-4 promotes angiogenesis and growth of glioblastoma multiforme by elevating matrix GLA levels

et al. 2010

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Inhibitor of differentiation-4 is highly expressed in glioblastoma multiforme (GBM). We report a novel proangiogenic function for inhibitor of differentiation-4 in the growth of glioblastoma xenografts. Tumor-derived cell cultures expressing elevated levels of ID4 produced enlarged xenografts in immunosuppressed mice that were better vascularized than corresponding control tumors and expressed elevated matrix GLA protein (MGP) that mediated enhanced tumor angiogenesis. Inhibition of MGP resulted in smaller and less vascularized xenografts. Our finding shows a novel function for ID4 in tumor angiogenesis, and identifies ID4 and MGP as possible therapeutic targets for GBM.

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Section: Id4 Elevates Mgp Promoting Gbm Growthmentioning

confidence: 96%

Section: Id4 Facilitates Growth Of Gbm Xenograftsmentioning

confidence: 99%

Section: Identification Of a Potential Id4 Target Promoting Angiogenementioning

confidence: 99%

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Inhibitor of DNA binding-4 promotes angiogenesis and growth of glioblastoma multiforme by elevating matrix GLA levels

et al. 2010

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“…Molecular mechanisms contributing to this pathology include a decrease in circulating and local inhibitors of mineralization, especially in dialysis patients with chronic kidney disease, as well as osteogenic and chondrogenic transformations of vascular smooth muscle cells (VSMCs) 2 that support calcification in the vascular wall via processes thought to recapitulate physiological ossification.…”

mentioning

confidence: 99%

Two Sides of MGP Null Arterial Disease

Beazley

Reckard

Nurminsky

et al. 2013

Journal of Biological Chemistry

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Background: MGP inhibits tissue calcification, but underlying mechanisms are understudied. Results: In MGP null mice, TG2 ablation prevents calcifying cartilaginous vascular lesions but does not affect elastocalcinosis and elastin fragmentation associated with increased elastase adipsin. Conclusion: MGP acts via two distinct mechanisms. Significance: Our study identifies TG2 and adipsin as potential therapeutic targets in vascular disease linked to MGP deficiency.

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“…Multiple stimuli, including hypoxia, cytokines, and growth factors, control VEGF expression (2). FGF-2 and TGF-␤1 induce endothelial cell expression of VEGF, which mediates the angiogenic activity of FGF-2 in vitro and in vivo (4,5).…”

mentioning

confidence: 99%

VEGF, a prosurvival factor, acts in concert with TGF-β1 to induce endothelial cell apoptosis

Ferrari

Pintucci

Seghezzi

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

142

147

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VEGF and TGF-␤1 are potent angiogenesis inducers with opposing effects on endothelial cells. TGF-␤1 induces apoptosis; VEGF protects endothelial cells from apoptosis. We found that TGF-␤1 promotes endothelial cell expression of FGF-2, which up-regulates VEGF synthesis. Inhibition of VEGF signaling through VEGF receptor 2 (flk-1) abrogates TGF-␤1-induced apoptosis and p38 MAPK activation. Inhibition of p38 MAPK blocks TGF-␤1-induced apoptosis, showing that VEGF͞flk-1-mediated activation of p38 MAPK is required for TGF-␤1 induction of apoptosis. In the absence of TGF-␤1, VEGF activates p38 MAPK and promotes endothelial cell survival. However, in context with TGF-␤1, VEGF͞flk-1-mediated activation of p38 MAPK results in apoptosis. Thus, cross-talk between TGF-␤1 and VEGF signaling converts VEGF͞flk-1-activated p38 MAPK into a proapoptotic signal. This finding illustrates an unexpected role of VEGF and indicates that VEGF can be pharmacologically converted into an apoptotic factor, a novel approach to antiangiogenesis therapy.angiogenesis ͉ MAPK kinase ͉ p38 ͉ VEGF receptor ͉ cancer

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Matrix GLA Protein Stimulates VEGF Expression through Increased Transforming Growth Factor-β1 Activity in Endothelial Cells

Cited by 105 publications

References 62 publications

Inhibitor of DNA binding-4 promotes angiogenesis and growth of glioblastoma multiforme by elevating matrix GLA levels

Inhibitor of DNA binding-4 promotes angiogenesis and growth of glioblastoma multiforme by elevating matrix GLA levels

Two Sides of MGP Null Arterial Disease

VEGF, a prosurvival factor, acts in concert with TGF-β1 to induce endothelial cell apoptosis

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