Neuropilin-2 is a receptor for the vascular endothelial growth factor (VEGF) forms VEGF-145 and VEGF-165.
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Tumor progression
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Neuropilin
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We have isolated and characterized a novel growth factor for endothelial cells, vascular endothelial growth factor B (VEGF-B), with structural similarities to vascular endothelial growth factor (VEGF) and placenta growth factor. VEGF-B was particularly abundant in heart and skeletal muscle and was coexpressed with VEGF in these and other tissues. VEGF-B formed cell-surface-associated disulfide-linked homodimers and heterodimerized with VEGF when coexpressed. Conditioned medium from transfected 293EBNA cells expressing VEGF-B stimulated DNA synthesis in endothelial cells. Our results suggest that VEGF-B has a role in angiogenesis and endothelial cell growth, particularly in muscle.
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Objective To determine the effect of PTK787 on the expression of vascular endothelial growth factor and vascular endothelial growth factor receptor-2 mRNA,and further discuss the role of PTK787 on anti-acute myeloid leukemia.Methods The acute myeloid leukemia model was established on 40 severe combined immunodeficiency mice by HL-60 cells transplantation.The mice were divided into five group randomly,the normal group,the sicken group,the treated group with 50mg/kg PTK787,the treated group with 100mg/kg PTK787,the treated group with 200mg/kg PTK787.Logarithmic phase cells were implanted into the sicken group and the treated group by celiac injection.The expression of vascular endothelial growth factor was detected by enzyme linked immunosorbent assay.The expression of vascular endothelial growth factor receptor-2 mRNA was detected by reverse transcription-polymerase chain reaction.Results(1)Expression of vascular endothelial growth factors and vascular endothelial growth factor receptor-2 mRNA were determined on all mice.(2)Compared with the normal group,the mRNA level of vascular endothelial growth factor and vascular endothelial growth factor receptor-2 in the sicken group was significantly and gradually increased with the course of disease.(3)Compared with the sicken group,the expression of vascular endothelial growth factor and vascular endothelial growth factor receptor-2 mRNA of treated group decreased obviously.Conclusion The anti-effect on acute myeloid leukemia of PTK787 is related with the decrease expression of vascular endothelial growth factor and vascular endothelial growth factor receptor-2.
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Vascular permeability
Lymphatic Endothelium
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Systemic vascular endothelial growth factor inhibition, in combination with chemotherapy, improves the outcome of patients with metastatic cancer. Peripheral sensory neuropathies occurring in patients receiving both drugs are attributed to the chemotherapy. Here, we provide unprecedented evidence that vascular endothelial growth factor receptor inhibitors trigger a painful neuropathy and aggravate paclitaxel-induced neuropathies in mice. By using transgenic mice with altered neuronal vascular endothelial growth factor receptor expression, systemic inhibition of vascular endothelial growth factor receptors was shown to interfere with the endogenous neuroprotective activities of vascular endothelial growth factor on sensory neurons. In vitro, vascular endothelial growth factor prevented primary dorsal root ganglion cultures from paclitaxel-induced neuronal stress and cell death by counteracting mitochondrial membrane potential decreases and normalizing hyperacetylation of α-tubulin. In contrast, vascular endothelial growth factor receptor inhibitors exerted opposite effects. Intriguingly, vascular endothelial growth factor or vascular endothelial growth factor receptor inhibitors exerted their effects through a mechanism whereby Hdac6, through Hsp90, controls vascular endothelial growth factor receptor-2-mediated expression of the anti-apoptotic Bcl2. Our observations that systemic anti-vascular endothelial growth factor therapies interfere with the neuroprotective activities of vascular endothelial growth factor may have important implications for the application of anti-vascular endothelial growth factor therapies in cancer patients.
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症例は58歳女性,下肢脱力と全身倦怠感を主訴に受診し,多発性神経炎,肝脾腫・甲状腺機能低下症, Mタンパク,皮膚硬化を認めPOEMS症候群と診断した.肺高血圧症の合併も認めた.ステロイドパルス療法を行い症状改善,治療前vascular endothelial growth factor (VEGF)の異常高値を認めたが治療後減少した. POEMS症候群は稀な疾患であるが, VEGFの推移を追跡し疾患活動性の指標として有用であったので報告する.
POEMS syndrome
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Background:Blocking vascular endothelial growth factor receptor (VEGFR) is a successful approach for inhibiting vascular endothelial growth factor (VEGF) signaling. Small molecules impairing the interaction of VEGF with VEGF receptors have been synthesized and evaluated in this research.
Blocking (statistics)
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