PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33405758-7 2019 The high therapeutic potential of cobalt nanoframework in the nanofibers enhanced the production of vascular endothelial growth factor promoting angiogenesis that resulted in the earlier restoration of wounded tissue compared with untreated control in vivo animal models. Cobalt 34-40 vascular endothelial growth factor A Homo sapiens 100-134 7933988-13 1994 As in vitro, cobalt was also found to be a potent stimulator of VEGF in vivo. Cobalt 13-19 vascular endothelial growth factor A Homo sapiens 64-68 32876363-0 2021 Cobalt-containing bioactive glass mimics VEGFA and HIF1A function. Cobalt 0-6 vascular endothelial growth factor A Homo sapiens 41-46 32876363-2 2021 Among the many ions that could be incorporated, cobalt (Co) is a significant one, as it mimics hypoxia, triggering the formation of new blood vessels by the vascular endothelial growth factor A (VEGFA), due to the stabilizing effect on the hypoxia inducible factor 1 subunit alpha (HIF1A), an activator of angiogenesis-related genes, and is therefore of great interest for tissue engineering applications. Cobalt 48-54 vascular endothelial growth factor A Homo sapiens 157-193 32876363-2 2021 Among the many ions that could be incorporated, cobalt (Co) is a significant one, as it mimics hypoxia, triggering the formation of new blood vessels by the vascular endothelial growth factor A (VEGFA), due to the stabilizing effect on the hypoxia inducible factor 1 subunit alpha (HIF1A), an activator of angiogenesis-related genes, and is therefore of great interest for tissue engineering applications. Cobalt 48-54 vascular endothelial growth factor A Homo sapiens 195-200 32876363-2 2021 Among the many ions that could be incorporated, cobalt (Co) is a significant one, as it mimics hypoxia, triggering the formation of new blood vessels by the vascular endothelial growth factor A (VEGFA), due to the stabilizing effect on the hypoxia inducible factor 1 subunit alpha (HIF1A), an activator of angiogenesis-related genes, and is therefore of great interest for tissue engineering applications. Cobalt 56-58 vascular endothelial growth factor A Homo sapiens 157-193 32876363-2 2021 Among the many ions that could be incorporated, cobalt (Co) is a significant one, as it mimics hypoxia, triggering the formation of new blood vessels by the vascular endothelial growth factor A (VEGFA), due to the stabilizing effect on the hypoxia inducible factor 1 subunit alpha (HIF1A), an activator of angiogenesis-related genes, and is therefore of great interest for tissue engineering applications. Cobalt 56-58 vascular endothelial growth factor A Homo sapiens 195-200 33451366-11 2021 Exposing fibroblasts to conditioned media from these composites did not cause a detrimental effect on metabolic activity but glasses containing cobalt did stabilise HIF-1alpha and provoked a significantly higher expression of VEGF (not seen in Co-free controls). Cobalt 144-150 vascular endothelial growth factor A Homo sapiens 226-230 29626696-0 2018 Fine-tuning pro-angiogenic effects of cobalt for simultaneous enhancement of vascular endothelial growth factor secretion and implant neovascularization. Cobalt 38-44 vascular endothelial growth factor A Homo sapiens 77-111 29626696-3 2018 In this study, we aimed at optimizing the pro-angiogenic effect of Cobalt (Co2+) to enhance vascular endothelial growth factor (VEGF) expression by human periosteum-derived mesenchymal stem cells (hPDCs). Cobalt 67-73 vascular endothelial growth factor A Homo sapiens 92-126 29626696-3 2018 In this study, we aimed at optimizing the pro-angiogenic effect of Cobalt (Co2+) to enhance vascular endothelial growth factor (VEGF) expression by human periosteum-derived mesenchymal stem cells (hPDCs). Cobalt 67-73 vascular endothelial growth factor A Homo sapiens 128-132 29626696-10 2018 STATEMENT OF SIGNIFICANT: Cobalt (Co2+) is known to upregulate vascular endothelial growth factor (VEGF) secretion, however it also inhibits in vitro angiogenesis through unknown Co2+-induced events. Cobalt 26-32 vascular endothelial growth factor A Homo sapiens 63-97 29626696-10 2018 STATEMENT OF SIGNIFICANT: Cobalt (Co2+) is known to upregulate vascular endothelial growth factor (VEGF) secretion, however it also inhibits in vitro angiogenesis through unknown Co2+-induced events. Cobalt 26-32 vascular endothelial growth factor A Homo sapiens 99-103 25818442-6 2015 Moreover, in vitro analysis demonstrated that the incorporation of cobalt bioactive glass with a mean particle size of 100 mum significantly enhanced the production and expression of VEGF in endothelial cells, and cobalt bioactive glass/collagen-glycosaminoglycan scaffold conditioned media also promoted enhanced tubule formation. Cobalt 67-73 vascular endothelial growth factor A Homo sapiens 183-187 28750600-10 2017 Finally, in static culture assays, the capacity of cobalt doping to induce vascular endothelial growth factor (VEGF) upregulation by osteoblastic cells was observed, but was not found to increase linearly with cobalt oxide content. Cobalt 51-57 vascular endothelial growth factor A Homo sapiens 75-109 28750600-10 2017 Finally, in static culture assays, the capacity of cobalt doping to induce vascular endothelial growth factor (VEGF) upregulation by osteoblastic cells was observed, but was not found to increase linearly with cobalt oxide content. Cobalt 51-57 vascular endothelial growth factor A Homo sapiens 111-115 11886167-2 2002 The expression of vascular endothelial growth factor (VEGF), a potent angiogenic factor, has been shown to be greatly stimulated in osteoblasts by hypoxic stimuli such as deprivation of oxygen and treatment with cobalt. Cobalt 212-218 vascular endothelial growth factor A Homo sapiens 18-52 24611881-11 2014 Sorafenib inhibited cobalt-induced HIF-1alpha and VEGFA expression in hepatoma cells. Cobalt 20-26 vascular endothelial growth factor A Homo sapiens 50-55 23840602-7 2013 Cobalt-alloy particles (1 um-diameter, 10 particles/cell) induced significantly elevated HIF-1alpha, VEGF, TNF-alpha and ROS expression in human primary macrophages whereas Titanium-alloy particles did not. Cobalt 0-6 vascular endothelial growth factor A Homo sapiens 101-105 16678800-5 2006 Here, we present evidence that carcinogenic metals such as arsenite, vanadate, and cobalt, induce AMPK activation and VEGF expression via several different mechanisms, and that AMPK is able to regulate the expression of VEGF mRNA in a hypoxia-inducible factor-1-dependent or -independent manner, depending on the metal applied. Cobalt 83-89 vascular endothelial growth factor A Homo sapiens 118-122 16678800-5 2006 Here, we present evidence that carcinogenic metals such as arsenite, vanadate, and cobalt, induce AMPK activation and VEGF expression via several different mechanisms, and that AMPK is able to regulate the expression of VEGF mRNA in a hypoxia-inducible factor-1-dependent or -independent manner, depending on the metal applied. Cobalt 83-89 vascular endothelial growth factor A Homo sapiens 220-224 12218411-8 2002 In the in vivo focal cerebral ischemia model and the in vitro hypoxic cell culture model with cobalt, BAI2 expression decreased after hypoxia and preceded the increased expression of vascular endothelial growth factor (VEGF). Cobalt 94-100 vascular endothelial growth factor A Homo sapiens 183-217 12218411-8 2002 In the in vivo focal cerebral ischemia model and the in vitro hypoxic cell culture model with cobalt, BAI2 expression decreased after hypoxia and preceded the increased expression of vascular endothelial growth factor (VEGF). Cobalt 94-100 vascular endothelial growth factor A Homo sapiens 219-223 12147617-5 2002 Treatment with cobalt was used to mimic hypoxia-induced expression of VEGF. Cobalt 15-21 vascular endothelial growth factor A Homo sapiens 70-74 16807025-3 2006 Cells were separately treated with cobalt ions (Co2+), basic fibroblast growth factor (bFGF), and estradiol (E2), which have been demonstrated to stimulate mammalian VEGF A expression, followed by quantification of the VEGF mRNA levels by real-time reverse transcription polymerase chain reaction. Cobalt 35-41 vascular endothelial growth factor A Homo sapiens 166-170 16249516-0 2005 Triamcinolone acetonide destabilizes VEGF mRNA in Muller cells under continuous cobalt stimulation. Cobalt 80-86 vascular endothelial growth factor A Homo sapiens 37-41 16249516-8 2005 VEGF mRNA decreased 50- to 100-fold 6 hours after treatment with TA and cobalt compared with cobalt alone. Cobalt 72-78 vascular endothelial growth factor A Homo sapiens 0-4 16249516-8 2005 VEGF mRNA decreased 50- to 100-fold 6 hours after treatment with TA and cobalt compared with cobalt alone. Cobalt 93-99 vascular endothelial growth factor A Homo sapiens 0-4 16249516-9 2005 VEGF mRNA stability was decreased in cobalt-stimulated, TA-treated cells compared with cobalt alone in cells synchronized by exposure to actinomycin D. Cobalt 37-43 vascular endothelial growth factor A Homo sapiens 0-4 16249516-9 2005 VEGF mRNA stability was decreased in cobalt-stimulated, TA-treated cells compared with cobalt alone in cells synchronized by exposure to actinomycin D. Cobalt 87-93 vascular endothelial growth factor A Homo sapiens 0-4 16249516-12 2005 CONCLUSIONS: TA may decrease VEGF synthesis by nongenomic destabilization of VEGF mRNA in cobalt-stimulated Muller cells. Cobalt 90-96 vascular endothelial growth factor A Homo sapiens 77-81 11886167-2 2002 The expression of vascular endothelial growth factor (VEGF), a potent angiogenic factor, has been shown to be greatly stimulated in osteoblasts by hypoxic stimuli such as deprivation of oxygen and treatment with cobalt. Cobalt 212-218 vascular endothelial growth factor A Homo sapiens 54-58 11886167-5 2002 Exposure of these cells to hypoxia or cobalt resulted in a great increase in the protein level of HIF-1alpha and the gene expression of VEGF. Cobalt 38-44 vascular endothelial growth factor A Homo sapiens 136-140 11886167-8 2002 In contrast, N-acetylcysteine (NAC), a scavenger of reactive oxygen species, abolished the cobalt induction of HIF-1alpha and that of the VEGF and a HRE-driven reporter genes. Cobalt 91-97 vascular endothelial growth factor A Homo sapiens 138-142 11886167-10 2002 These findings suggest that hypoxia and cobalt can induce VEGF gene expression in osteoblasts by increasing the level of HIF-1alpha protein through different mechanisms. Cobalt 40-46 vascular endothelial growth factor A Homo sapiens 58-62 10606981-4 2000 VEGF was quantified in cell culture supernatants after stimulation with lipopolysaccharide (LPS), PlGF or cobalt ions of PBMC isolated from RA patients and controls. Cobalt 106-112 vascular endothelial growth factor A Homo sapiens 0-4 10751333-7 2000 In addition, we analyzed the effects of nickel and cobalt on the expression of VEGF in osteoblastic cells because these metallic ions mimic hypoxia by binding to the heme portion of oxygen-sensing molecules. Cobalt 51-57 vascular endothelial growth factor A Homo sapiens 79-83 10751333-9 2000 In addition, we found that nickel and cobalt both stimulate VEGF gene expression in a similar time- and dose-dependent manner, suggesting the presence of a hemelike oxygen-sensing mechanism similar to that of the EPO gene. Cobalt 38-44 vascular endothelial growth factor A Homo sapiens 60-64 10751333-11 2000 These studies demonstrate that hypoxia, nickel, and cobalt regulate VEGF expression in osteoblasts via a similar mechanism, implicating the involvement of a heme-containing oxygen-sensing molecule. Cobalt 52-58 vascular endothelial growth factor A Homo sapiens 68-72 10971326-7 2000 Irradiation of TGF-beta1-stimulated fibroblasts resulted in a synergistic effect on increasing levels of VEGF but not ET-1 after 48 h. Cobalt chloride stimulated the secretion of VEGF by fibroblasts; the effects of TGF-beta1 and cobalt were additive. Cobalt 229-235 vascular endothelial growth factor A Homo sapiens 179-183