Aggregating Human Platelets Stimulate Expression of Vascular Endothelial Growth Factor in Cultured Vascular Smooth Muscle Cells Through a Synergistic Effect of Transforming Growth Factor-β
            <sub>1</sub>
            and Platelet-Derived Growth Factor
            <sub>AB</sub>

Kronemann, Nicola; Bouloumié, Anne; Bassus, S.; Kirchmaier, C. M.; Busse, Rudi; Schini‐Kerth, Valérie B.

doi:10.1161/01.cir.100.8.855

Cited by 27 publications

(21 citation statements)

References 25 publications

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“…9,10 Kamihata et al 11 and Shintani et al 12 have shown that BM mononuclear cells (BM-MNCs) contain not only EPCs but also angiogenic factors and cytokines and that implantation of BM-MNCs into ischemic tissues augments collateral vessel formation. Peripheral blood mononuclear cells (PBMNCs), 13 polymorphonuclear leukocytes (PMNs), 14 and platelets 15,16 synthesize and release high levels of VEGF as well as PDGF and transforming growth factor (TGF)-␤, known to be prerequisites for the investment of stable vessels with pericytes. 17 PMNs have also been shown to release various angiogenic cytokines, including interleukin (IL)-1, IL-6, IL-8, and tumor necrosis factor-␣, 18 and MMPs 19 and to enhance proliferation and tubule formation of endothelial cells in vitro.…”

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confidence: 99%

Angiogenesis by Implantation of Peripheral Blood Mononuclear Cells and Platelets Into Ischemic Limbs

et al. 2002

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Background-Peripheral PϽ0.01). Neocapillary densities were increased by implantation of PBMNCsϩplatelets or platelets alone (3.5-fold and 2.4-fold, respectively; PϽ0.001), whereas PMNs inhibited (32%, PϽ0.05) PBMNCϩplatelet-mediated capillary formation. There was no incorporation of implanted PBMNCs into neocapillaries, whereas PBMNCs and platelets accumulated around arterioles after implantation. Cellular extract from PBMNCsϩplatelets, in which vascular endothelial growth factor (VEGF), basic fibroblast growth factor, platelet-derived growth factor-AB, and transforming growth factor-␤ were detected, markedly stimulated tubule formation of human umbilical vein vascular endothelial cells. Anti-VEGF neutralizing antibody markedly inhibited tubule formation and in vivo vessel formation. Neutrophil elastase inhibitor blocked the antiangiogenic action of PMNs, whereas inhibitors of oxygen metabolites had no effect. Conclusions-This study demonstrated that implantation of PBMNCs and platelets into ischemic limbs effectively induces collateral vessel formation by supplying angiogenic factors (mainly VEGF) and cytokines, suggesting that this cell therapy is useful as a novel strategy for therapeutic angiogenesis.

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confidence: 99%

Angiogenesis by Implantation of Peripheral Blood Mononuclear Cells and Platelets Into Ischemic Limbs

et al. 2002

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“…VEGF 165 may act as a paracrine hormone to stimulate migration and proliferation of endothelial cells (21). However, TGF-␤ 1 may induce VEGF 165 expression (8) and synergistically with TGF-␤ 1 may increase vascular SMC proliferation (44).…”

Section: Discussionmentioning

confidence: 99%

Ovariectomy increases mitogens and platelet-induced proliferation of arterial smooth muscle

Bracamonte¹,

Rud²,

Owen

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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-Experiments were designed to determine how ovariectomy modulates mitogenic factors in platelets and how these factors affect proliferation of coronary arterial smooth muscle. Platelet-derived growth factors (PDGFAB and PDGFBB), transforming growth factors (TGF-␤1 and TGF-␤2), and vascular endothelial growth factor (VEGF165) were quantified in platelet lysates and platelet-poor plasma from adult gonadally intact and ovariectomized female pigs by ELISA. Proliferation of cultured coronary arterial smooth muscle cells (SMCs) from both groups of pigs was determined in response to autologous or heterologous platelet lysates. Platelet concentrations of PDGFBB, but not PDGFAB, TGF-␤1, and TGF-␤2, increased with ovariectomy. VEGF165 was not detected in platelets from either group. Proliferation of SMCs from ovariectomized females was significantly greater on exposure to autologous or heterologous platelet lysates than proliferation of SMCs from intact females. These results indicate that ovariectomy increases concentrations of PDGFBB in platelets. Higher levels of PDGFBB in platelets in synergy with other plateletderived products could contribute to increased proliferative arterial response to injury after ovariectomy.

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“…4 Hybridizations were carried out with 32 Plabeled rat p22 phox , 4 rat VEGF, 22 or digoxigenin-labeled rat PAI-1 and ␤-actin cDNA probes. 18 …”

Section: Northern Blotmentioning

confidence: 99%

“…Because thrombin, activated platelets, and platelet-associated growth factors enhance the mRNA expression of the HIF-1 target genes VEGF and PAI-1 in VSMCs, [22][23][24] activation of HIF-1 may represent a novel mechanism by which thrombotic factors regulate gene expression in the vascular wall. Inhibition of thrombin-induced expression, nuclear accumulation, and transactivation of HIF-1␣ by the antioxidants vitamin C, vitamin E, trolox, NAC, and PDTC indicated redox-sensitive mechanisms involved in this signaling pathway.…”

Section: Görlach Et Al Thrombin Induces Hif-1␣mentioning

confidence: 99%

“…Indeed, thrombotic factors, including activated platelets, platelet-associated growth factors, and thrombin, can upregulate these genes in VSMCs. [22][23][24] Moreover, exposure to ROS enhanced VEGF expression in VSMCs 13 and induced PAI-1 accumulation in rat heart microvessels. 25 We therefore hypothesized that thrombotic factors can activate the HIF-1 signaling pathway and that the generation of ROS may contribute to this response.…”

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Thrombin Activates the Hypoxia-Inducible Factor-1 Signaling Pathway in Vascular Smooth Muscle Cells

Görlach

Diebold

Schini‐Kerth

et al. 2001

Circulation Research

380

304

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Abstract-The heterodimeric transcription factor hypoxia-inducible factor-1 (HIF-1) is activated under hypoxic conditions, resulting in the upregulation of its target genes plasminogen activator inhibitor-1 (PAI-1) and vascular endothelial growth factor (VEGF). PAI-1 and VEGF are also induced in response to vascular injury, which is characterized by the activation of platelets and the coagulation cascade as well as the generation of reactive oxygen species (ROS). However, it is not known whether HIF-1 is also stimulated by thrombotic factors. We investigated the role of thrombin, platelet-associated growth factors, and ROS derived from the p22 phox -containing NADPH oxidase in the activation of HIF-1 and the induction of its target genes PAI-1 and VEGF in human vascular smooth muscle cells (VSMCs). Thrombin, platelet-derived growth factor-AB (PDGF-AB), and transforming growth factor-␤ 1 (TGF-␤ 1 ) upregulated HIF-1␣ protein in cultured and native VSMCs. This response was accompanied by nuclear accumulation of HIF-1␣ as well as by increased HIF-1 DNA-binding and reporter gene activity. The thrombin-induced expression of HIF-1␣, PAI-1, and VEGF was attenuated by antioxidant treatment as well as by transfection of p22 phox antisense oligonucleotides. Inhibition of p38 mitogen-activated protein kinase and phosphatidylinositol-3-kinase significantly decreased thrombin-induced HIF-1␣, PAI-1, and VEGF expression. These findings demonstrate that the HIF-1 signaling pathway can be stimulated by thrombin and platelet-associated growth factors and that a redox-sensitive cascade activated by ROS derived from the p22 phox -containing NADPH oxidase is crucially involved in this response. Key Words: oxygen radicals Ⅲ p22 phox Ⅲ platelets Ⅲ vascular endothelial growth factor Ⅲ plasminogen activator inhibitor-1

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Aggregating Human Platelets Stimulate Expression of Vascular Endothelial Growth Factor in Cultured Vascular Smooth Muscle Cells Through a Synergistic Effect of Transforming Growth Factor-β ₁ and Platelet-Derived Growth Factor _AB

Cited by 27 publications

References 25 publications

Angiogenesis by Implantation of Peripheral Blood Mononuclear Cells and Platelets Into Ischemic Limbs

Angiogenesis by Implantation of Peripheral Blood Mononuclear Cells and Platelets Into Ischemic Limbs

Ovariectomy increases mitogens and platelet-induced proliferation of arterial smooth muscle

Thrombin Activates the Hypoxia-Inducible Factor-1 Signaling Pathway in Vascular Smooth Muscle Cells

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Aggregating Human Platelets Stimulate Expression of Vascular Endothelial Growth Factor in Cultured Vascular Smooth Muscle Cells Through a Synergistic Effect of Transforming Growth Factor-β 1 and Platelet-Derived Growth Factor AB

Cited by 27 publications

References 25 publications

Angiogenesis by Implantation of Peripheral Blood Mononuclear Cells and Platelets Into Ischemic Limbs

Angiogenesis by Implantation of Peripheral Blood Mononuclear Cells and Platelets Into Ischemic Limbs

Ovariectomy increases mitogens and platelet-induced proliferation of arterial smooth muscle

Thrombin Activates the Hypoxia-Inducible Factor-1 Signaling Pathway in Vascular Smooth Muscle Cells

Contact Info

Product

Resources

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Aggregating Human Platelets Stimulate Expression of Vascular Endothelial Growth Factor in Cultured Vascular Smooth Muscle Cells Through a Synergistic Effect of Transforming Growth Factor-β ₁ and Platelet-Derived Growth Factor _AB