• Secreted VEGF binds to VEGFR on endothelial cells and enhances their proliferation and migration toward the tumor site. (medscape.com)
  • VEGF binds to and activates a receptor tyrosine kinase, VEGFR, through transphosphorylation. (tocris.com)
  • VEGFR-2 is a 210-230 kDa glycoprotein expressed in vascular endothelial cells and in hematopoietic stem cells and binds VEGF-A. VEGFR-2 is closely related to VEGFR-1 for they have common and specific ligands but VEGFR-2 is a highly active kinase while VEGFR1 is an impaired receptor tyrosine kinase. (wikipedia.org)
  • Bevacizumab is a humanized monoclonal antibody, which binds selectively to VEGF. (wikipedia.org)
  • Vascular endothelial growth factor B (VEGF-B) binds to VEGF receptor-1 and regulates plasminogen activator activity in endothelial cells. (smw.ch)
  • and dose dependently binds to VEGF receptor 1 (VEGFR1) and VEGF receptor 2 (VEGFR2) as observed Quisinostat by ELISA. (ikk-signaling.com)
  • Vascular endothelial growth factor receptor 2 (VEGFR2) antagonist that specifically binds VEGF receptor 2 and blocks binding of VEGFR ligands, VEGF-A, VEGF-C, and VEGF-D. As a result, ramucirumab inhibits ligand-stimulated activation of VEGF2, thereby inhibiting ligand-induced proliferation, and migration of human endothelial cells. (medscape.com)
  • VEGFR-2 selective inhibitor can interrupt multiple signaling pathways involved in tumor, including proliferation, metastasis and angiogenesis. (wikipedia.org)
  • ING5 overexpression suppressed growth, blood supply and lung metastasis of SGC-7901 cells by inhibiting proliferation, enhancing autophagy and apoptosis in xenograft models. (oncotarget.com)
  • It was suggested that ING5 expression might be employed as a good marker for gastric carcinogenesis and subsequent progression by inhibiting proliferation, growth, migration, invasion and metastasis. (oncotarget.com)
  • Previous studies have shown that VEGF and HIF-1α play an important role in tumor growth, angiogenesis, metastasis, and apoptosis. (kosinmedj.org)
  • However, combining SC236 and VEGF inhibition significantly reduced the incidence of lung metastasis, suggesting a distinct effect on prometastatic mechanisms. (biomedcentral.com)
  • Collectively, these findings suggest that during VEGF blockade COX-2 may restrict metastasis by limiting both prometastatic behaviors in individual tumor cells and mobilization of macrophages to the tumor vasculature. (biomedcentral.com)
  • Both clinical and experimental studies indicate that many or most malignancies will ultimately progress if VEGF blockade is sustained, and that progression may involve both progressive primary tumor growth and enhanced metastasis. (biomedcentral.com)
  • Thus, it is not known whether the addition of SC236 would limit spontaneous lung metastasis in hypoperfused tumors as occurs during VEGF blockade, when primary tumor angiogenesis is restricted but other prometastatic mechanisms may be active. (biomedcentral.com)
  • Over the past few years, more and more studies have paid close attention to the role of angiogenesis, including the imbalance between anti-angiogenic and pro-angiogenic effects, in OS progression including proliferation, migration, and metastasis [ 8 ]. (ijbs.com)
  • GM-CSF promoted migration and differentiation of MDSCs, which inhibited the CD8 + lymphocyte proliferation. (nature.com)
  • Mesenchymal stem cells (MSCs) are multipotent stem cells with abundant source, active proliferation, and multidirectional differentiation potential. (hindawi.com)
  • ING5 suppresses proliferation, apoptosis, migration and invasion, and induces autophagy and differentiation of gastric cancer cells: a good marker for. (oncotarget.com)
  • Although the pathogenic pathways involved in IPF have not been fully elucidated, IPF is believed to be caused by repetitive alveolar epithelial cell injury and dysregulated repair, in which there is uncontrolled proliferation of lung fibroblasts and differentiation of fibroblasts into myofibroblasts, which excessively deposit extracellular matrix (ECM) proteins in the interstitial space. (ersjournals.com)
  • Data from in vitro studies have shown that nintedanib interferes with processes active in fibrosis such as fibroblast proliferation, migration and differentiation, and the secretion of ECM. (ersjournals.com)
  • We will further study how the interaction affects endothelial cell, migration, proliferation, and differentiation. (nih.gov)
  • Plays a role in cell adhesion, migration, proliferation and differentiation. (nih.gov)
  • Certain circRNAs, such as circRNA ankyrin repeat domain 36, circRNA homeodomain‑interacting protein kinase 3 (circHIPK3) and circRNA WD repeat domain 77, are associated with inflammation, endothelial cell apoptosis and smooth muscle cell proliferation, leading to vascular endothelial dysfunction and atherosclerosis. (spandidos-publications.com)
  • CircRNA LDL receptor related protein 6, circRNA actin related protein 2, circ_0000064, circ‑0101383, circ_0123996, hsa_circ_0003928 and circ_0000285 mediate inflammation, apoptosis and autophagy of podocytes, mesangial cell hypertrophy and proliferation, as well as tubulointerstitial fibrosis, in diabetic nephropathy by regulating the expression of microRNAs and proteins. (spandidos-publications.com)
  • It has been speculated that OI may directly or indirectly induce apoptosis of HepG2 cells by regulating apoptosis-related genes. (biomedcentral.com)
  • Mesenchymal stem cells have anti-angiogenic effects by inducing apoptosis in endothelial cells, inhibiting proangiogenic elements, and impeding migration in endothelial cells. (amparinhibitor.com)
  • Direct get in touch with of endothelial cells and MSCs leads to the transfer of mitochondria of MSCs to endothelial cells, increasing ROS goods in endothelial cells and consequently inducing apoptosis (Otsu et al. (amparinhibitor.com)
  • 2015). Besides, it has been observed that LL-37 induces vascular smooth muscle cell apoptosis via escalating the plasma membrane permeability (Ciornei et al. (amparinhibitor.com)
  • VEGF can bind to the FLT1/VEGFR1 and KDR/VEGFR2 receptors, heparan sulfate and heparin, and play important roles in inducing endothelial cell proliferation, promoting cell migration, inhibiting apoptosis and inducing permeabilization of blood vessels. (absin-reagents.com)
  • The anti-VEGF therapy induces tumour hypoxia and GM-CSF expression, which recruits MDSCs and inhibits tumour immunity. (nature.com)
  • Hypoxic conditions activate hypoxia-inducible factor 1 (HIF-1), resulting in increased VEGF mRNA expression. (tocris.com)
  • 8. Hypoxia-induced mitogenic factor enhances angiogenesis by promoting proliferation and migration of endothelial cells. (nih.gov)
  • We have recently demonstrated that the G-protein estrogen receptor (GPER) cooperates with hypoxia inducible factor-1α (HIF-1α) toward the regulation of the pro-angiogenic factor VEGF. (oncotarget.com)
  • 2006). Altogether, AMPs could disturb angiogenesis and avoid tumor development and invasion through inducing hypoxia and nutrition poverty inside the tumor atmosphere.ImmunomodulationMostly, the immune technique plays an essential function in controlling the growth of tumoral cells. (amparinhibitor.com)
  • In this study, we investigated inhibition of angiogenesis using Genipin-mediated hypoxia-induced hypoxia inducible factor (HIF-1) and VEGF expression in human cervical cancer cells. (kosinmedj.org)
  • Luciferase reporter assays were used to investigate the molecular mechanisms underlying the hypoxia-induced survivin activation. (kosinmedj.org)
  • Genipin treatment also significantly reduced hypoxia-induced secretion of VEGF. (kosinmedj.org)
  • VEGF expression is mainly regulated by hypoxia inducible factor 1 (HIF-1) at the transcriptional level. (kosinmedj.org)
  • Current study shows that microRNA-210 (miR-210) promotes vascular endothelial cell migration and tube formation under hypoxia in vitro. (nih.gov)
  • We found that SC236 limited tumor cell viability and migration in vitro , with effects enhanced by hypoxia, but did not change tumor proliferation or matrix metalloproteinase expression in vivo . (biomedcentral.com)
  • In this study, we confirm that MALAT1 induces pro-angiogenic effects, and demonstrate that the underlying mechanism involves a MALAT1/mechanistic target of rapamycin (mTOR)/hypoxia inducible factor-1α (HIF-1α) loop. (ijbs.com)
  • VEGFR-2 mediates the majority of cellular responses to VEGF, in particular its mitogenic and angiogenic effects. (tocris.com)
  • VEGFR-1 is thought to modulate VEGFR-2 signaling or to act as a dummy/decoy receptor to sequester VEGF away from VEGFR-2. (tocris.com)
  • The VEGF receptor family contains three members, which are all receptor tyrosine kinases (VEGFR-1, VEGFR-2 and VEGFR-3). (wikipedia.org)
  • Binding of VEGF to the VEGFR induces a conformational change in the receptor producing a signaling pathway. (wikipedia.org)
  • The signaling pathways, Y1175 and Y1214, are the main autophosphorylation sites of the human VEGFR-2 followed by VEGF binding. (wikipedia.org)
  • VEGFR-2 are a part of the VEGF family. (wikipedia.org)
  • VEGFR-2 inhibition augments cigarette smoke-induced oxidative stress and inflammatory responses leading to endothelial dysfunction. (nih.gov)
  • Vascular endothelial growth factor (VEGF) induces phosphorylation of VEGF receptor-2 (VEGFR-2) and activates the downstream signaling pathway resulting in endothelial cell migration, proliferation, and survival. (nih.gov)
  • Herein, we investigated the mechanism of cigarette smoke (CS) -induced endothelial dysfunction by studying the VEGF-VEGFR-2 signaling in mouse lung and human endothelial cells. (nih.gov)
  • Inhibition of VEGFR-2 by a specific kinase inhibitor (NVP-AAD777) enhanced the CS-induced oxidative stress, causing augmented inflammatory cell influx and proinflammatory mediators release in mouse lung. (nih.gov)
  • CS down-regulated VEGFR-2 expression, eNOS levels, and VEGF-induced VEGFR-2 phosphorylation in HMVEC-Ls, resulting in impaired VEGF-induced endothelial cell migration and angiogenesis. (nih.gov)
  • Here we review recent experiments showing how VEGFR-2 is transported through intracellular vesicular compartments specified by Rab family GTPases, and discuss how different VEGF-A isoforms specify intracellular receptor trafficking. (smw.ch)
  • We are also studying the mechanism of the anti-angiogenic activity of Fbln7-C. Our preliminary data showed that Fbln7-C bound to the vascular endothelial growth factor receptor (VEGFR), suggesting that inhibition of VEGF signaling is involved in Fbln7-mediated anti-angiogenic activity. (nih.gov)
  • Whilst multiple receptors and ligands are involved in angiogenesis, VEGF signaling is one of the most important, rate-limiting steps of the process. (tocris.com)
  • Sunitinib is an oral drug that inhibits the phosphorylation of all the VEGF receptors, PDGFR-ß, KIT FLT3, CSF1R and GDNF. (wikipedia.org)
  • This gene encodes one of the two receptors of the VEGF. (nih.gov)
  • Stuttfeld E, Ballmer-Hofer K. Structure and function of VEGF receptors. (smw.ch)
  • Neufeld G, Kessler O, Herzog Y. The interaction of Neuropilin-1 and Neuropilin-2 with tyrosine-kinase receptors for VEGF. (smw.ch)
  • Functional interaction of VEGF-C and VEGF-D with neuropilin receptors. (smw.ch)
  • A variety of chemokine receptors are expressed on the surface of both tumor and immune cells rendering them sensitive to multiple stimuli that can subsequently influence their migration and function. (frontiersin.org)
  • Chemokine receptors (red) influence melanoma tumor cell migration/invasion or immune cell trafficking to the tumor lesions. (frontiersin.org)
  • Inhibits the kinase activities of various subtypes of vascular endothelial growth factor (VEGF) receptors. (medscape.com)
  • They induce cellular functions common to other growth factor receptors such as cell migration, survival, and proliferation. (umbc.edu)
  • 1 , 5 , 6 The amount and duration of VEGF needed to pass through the blood-brain barrier are possibly less than the concentrations needed to induce neovascularization. (dovepress.com)
  • VEGF is diffusible and selective for vascular endothelial cells, and possesses the ability to promote the growth and survival of these cells in vitro . (tocris.com)
  • It also induces cell migration, proliferation and survival. (tocris.com)
  • It functions as the main mediator of VEGF-induced endothelial proliferation, survival, migration, tubular morphogenesis and sprouting. (nih.gov)
  • 13. Vaccarin promotes endothelial cell proliferation in association with neovascularization in vitro and in vivo. (nih.gov)
  • The neovascularization process in the retina depends on the growth factor production induced by hypoxic condition. (dovepress.com)
  • The implant with pro-angiogenic lipid 7-ketocholesterol (7KCh) alone started to induce neovascularization from the limbus. (nih.gov)
  • In HCC, effective strategies to block cancer cell migration, invasion, and neovascularization need to be further studied. (biomedcentral.com)
  • We designed microfluidic chips for cell migration, invasion, and neovascularization to evaluate the effect of OI on HepG2 cells. (biomedcentral.com)
  • Our findings suggest that OI may inhibit the migration, invasion, and neovascularization of HepG2 cells, and its regulatory mechanism may be related to the regulation of the P53 and VEGF pathways. (biomedcentral.com)
  • The anti-angiogenic effects of BRE were assessed on cell migration, proliferation and tube formation following VEGF stimulation as well as on activation of Akt, MAPK and JNK signaling pathways. (nih.gov)
  • Ligand-induced receptor is internalised and then transported through early, late, and recycling endosomes, and finally degraded by proteasomal or lysosomal pathways. (smw.ch)
  • ING5 might induce apoptotic and chemotherapeutic resistances of gastric cancer cells by activating β-catenin, NF-κB and Akt pathways. (oncotarget.com)
  • According to the P53 and VEGF pathways predicted by network pharmacology, RT‒qPCR and immunofluorescence staining experiments were conducted. (biomedcentral.com)
  • Unraveling these new pathways of exosome-initiated EC regulation could provide new options for therapeutic interference with tumor-induced angiogenesis. (unibas.ch)
  • Although it has been reported that treating cells with BFA interferes with Arf1 activation to inhibit VEGF secretion, the role of BIG1 and BIG2 in VEGF trafficking and expression, EC migration and proliferation, and vascular development remains unknown. (nih.gov)
  • These agents inhibit cell growth and proliferation. (medscape.com)
  • 2020). Furthermore, MSC-derived exosomes inhibit the expression of VEGF in TME by way of their microRNA-16 content (Lee et al. (amparinhibitor.com)
  • It has been observed that defensins could inhibit the migration of endothelial cells. (amparinhibitor.com)
  • These finding suggest that inhibition of VEGF signaling is one possible antiangiogenic mechanism of EMAP II, which may explain its in vivo antitumor activity and delineate therapeutic strategies to enhance anti-VEGF therapy to inhibit tumor growth. (ikk-signaling.com)
  • In addition, in human endothelial cells, the conditioned medium from breast cancer cells treated with CuSO 4 promoted cell migration and tube formation through HIF-1α and GPER. (oncotarget.com)
  • Gene set expression analysis (GSEA) indicated that the addition of SC236 to VEGF inhibition significantly reduced expression of gene sets linked to macrophage mobilization. (biomedcentral.com)
  • Perivascular recruitment of macrophages induced by VEGF blockade was disrupted in tumors treated with combined VEGF- and COX-2-inhibition. (biomedcentral.com)
  • Other growth factors such as EGF, TGF-β and PDGF may also upregulate VEGF expression. (tocris.com)
  • This gene is a member of the PDGF/VEGF growth factor family. (nih.gov)
  • This study aimed to investigate the concentrations of vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) in vitreous and serum samples, analyze the ratio, and compare among proliferative diabetic retinopathy (PDR) subgroups. (dovepress.com)
  • The VEGF-A and PDGF-AB concentrations were calculated by enzyme-linked immunosorbent assay. (dovepress.com)
  • The vitreous VEGF-A/PDGF-AB concentration ratios were also significantly different among the PDR subgroups. (dovepress.com)
  • High concentrations of VEGF and PDGF in vitreous samples of PDR eyes indicate its local related activity in PDR pathology. (dovepress.com)
  • The VEGF/PDGF concentration ratios possibly play a significant role in the formation of fibrotic tissue in PDR. (dovepress.com)
  • 9 - 11 Both VEGF and PDGF have very similar characteristics. (dovepress.com)
  • 2 , 3 PDGF could directly trigger cellular proliferation and movement. (dovepress.com)
  • There are five VEGF ligands in mammals, which bind, in an overlapping pattern to the three VEGFRs, which can form homo or heterodimers. (umbc.edu)
  • Several anti-angiogenic therapeutic agents are currently being investigated in clinical trials for the treatment of NSCLC, for example, the anti-VEGF antibody bevacizumab and the TKI sorafenib. (medscape.com)
  • Recombinant humanized monoclonal antibody to VEGF. (medscape.com)
  • BRE exerted differential anti-inflammatory effects between HEMEC and HIMEC following TNF-α/IL-1β activation whereas demonstrated similar anti-angiogenic effects following VEGF stimulation in both cell lines. (nih.gov)
  • VEGF signaling pathway is involved in embryonic vascular development (vasculogenesis) and in the formation of new blood vessel (angiogenesis). (tocris.com)
  • OI blocks the VEGF signaling pathway by downregulating the expression levels of VEGF, HIF-1α and EGFR and inhibits the migration and invasion of HepG2 cells and the formation of new blood vessels. (biomedcentral.com)
  • The increased expression levels of VEGF in solid tumors, hematological malignancies, age-related macular degeneration (AMD), diabetes mellitus and various inflammatory disorders has placed great emphasis on developing VEGF inhibitors. (tocris.com)
  • Migration to, and infiltration of, tumors by immune cells is critical for achieving this goal. (frontiersin.org)
  • Tumor-derived exosomes containing the tetraspanin Tspan8 can efficiently induce angiogenesis in tumors and tumor-free tissues. (unibas.ch)
  • Here, we found that inactivation of Arf1 reduced VEGF secretion but did not affect the levels of VEGF protein. (nih.gov)
  • Induces a cascade of intracellular signals that involves tyrosine kinase-dependent calcium mobilization, inositol triphosphate production and secretion of IL6 and CSF1. (transcriptionfactor.org)
  • BRE attenuated VEGF-induced cell migration, proliferation and tube formation in both HEMEC and HIMEC. (nih.gov)
  • 7. Insulin-like growth factor binding protein-7 (IGFBP7) blocks vascular endothelial cell growth factor (VEGF)-induced angiogenesis in human vascular endothelial cells. (nih.gov)
  • VEGF stimulates the formation of new blood vessels by inducing endothelial cell (EC) proliferation and migration. (nih.gov)
  • Biological output by VEGF is mediated through distinct receptor/co-receptor complexes and generates signals in all cellular compartments triggering cellular responses such as cell migration, cell proliferation, vessel formation and maturation, as well as changes in vessel fenestration, constriction and permeability. (smw.ch)
  • Many chemokines are constantly expressed and participate in the maintenance of tissue integrity, while some chemokines are transiently overexpressed or specifically induced in certain conditions (i.e., during inflammatory processes) where they are involved in critical biological functions (i.e., immune cell migration, tissue repair, cell proliferation and angiogenesis) ( 10 , 13 , 14 ). (frontiersin.org)
  • CNT-induced fibrosis involves a multitude of cell types and is characterized by the early onset of inflammation, oxidative stress and accumulation of extracellular matrix. (cdc.gov)
  • It inhibits endothelial cell proliferation and migration [5]. (who.int)
  • Thereby, regulates different biological processes including the organization of the cytoskeleton, cell migration and proliferation. (cusabio.com)
  • Negative regulator of cell proliferation. (nih.gov)
  • Compared to the control group, cell migration, invasion, and angiogenesis were significantly reduced in each administration group. (biomedcentral.com)
  • Trifluridine is a thymidine-based nucleoside analog that incorporates into DNA, interferes with DNA synthesis, and inhibits cell proliferation. (medscape.com)
  • Vascular endothelial growth factor (VEGF) is the primary inducer of angiogenesis and tumor cell proliferation and migration both in vivo and in vitro. (kosinmedj.org)
  • Among the ​plasma proteins, the molecules vital for the coagulation process and for the fibrin polymer formation will serve as a scaffold for cell migration and new tissue generation. (pt-itech.com)
  • Following 28 days of miR-210 gene transfer, endothelial cell and neural precursor cell proliferation, microvessel density and downstream angiogenic factor were genotyped. (nih.gov)
  • Eligible in vitro studies included single-cell and co-culture models to evaluate the proliferation, migration, and/or invasion of endometrial cells. (nih.gov)
  • In vitro evidence supported TCDD's promotion of cell migration and invasion, but there was insufficient evidence for cell proliferation. (nih.gov)
  • Profibrotic growth factors and cytokines contribute directly to fibroblast proliferation and collagen production. (cdc.gov)
  • Binding to VEGF receptor induces dimerization, which modifies the conformation in the intracellular domain. (wikipedia.org)
  • We investigated the relationship of VEGF as an angiogenic growth factor and endostatin as an angiogenic inhibitor in patients with pre-eclampsia. (who.int)
  • Sorafenib, a multikinase VEGF inhibitor, is the most widely used systemic chemotherapy agent. (biomedcentral.com)
  • VEGF expression is correlated with poor prognosis in NSCLC. (medscape.com)
  • BRE inhibited TNF-α/IL-1β-induced NFκB p65 nuclear translocation, PGE2 production, up-regulation of COX-2, ICAM-1 and VCAM-1 gene and protein expression and leukocyte binding in HEMEC but not in HIMEC. (nih.gov)
  • Here, we show that copper sulfate (CuSO 4 ) induces the expression of HIF-1α as well as GPER and VEGF in breast and hepatic cancer cells through the activation of the EGFR/ERK/c-fos transduction pathway. (oncotarget.com)
  • Oxygen tension and cytokines have been shown to influence trophoblast VEGF expression, suggesting that this particular family of angiogenic proteins plays an important role in placental angiogenesis [3]. (who.int)
  • Under normoxic and hypoxic conditions, the expression of HIF-1α and VEGF in cervical cancer HeLa cells was detected by quantitative reverse transcription polymerase chain reaction and western blotting. (kosinmedj.org)
  • 8 9 It has been well established that PI3K/AKT signaling is required for VEGF expression through HIF-1 in response to growth factor stimulation and oncogene activation. (kosinmedj.org)
  • Immunohistochemical analysis was conducted to identify CD34 and vascular endothelial growth factor (VEGF) expression. (medscimonit.com)
  • From NCBI Gene: Vascular endothelial growth factor (VEGF) is a major growth factor for endothelial cells. (nih.gov)
  • The rat VEGF protein contains a putative 20 amino acids (aa) signal peptide, and alternative splicing of rat VEGF gene produces isoforms of 120, 144, 164 and 188 aa. (absin-reagents.com)
  • VEGF gene transcription was detected with RT-PCR. (medscimonit.com)
  • The results showed that not only placental cells but also sub-cultured placental tissue, to some extent, promoted HUVEC angiogenesis in vitro by promoting proliferation, adhesion, migration, invasion, and tube formation. (biomedcentral.com)
  • 14. Requirement of the nuclear localization of transcription enhancer factor 3 for proliferation, migration, tube formation, and angiogenesis induced by vascular endothelial growth factor. (nih.gov)
  • 17. Adiponectin inhibits vascular endothelial growth factor-induced migration of human coronary artery endothelial cells. (nih.gov)
  • This growth factor induces proliferation and migration of vascular endothelial cells, and is essential for both physiological and pathological angiogenesis. (nih.gov)
  • 1 Vascular endothelial growth factor (VEGF) is a dominant proangiogenic factor in proliferative diabetic retinopathy (PDR), which triggers migration and proliferation of endothelial cells and blood flow increase, together with microvascular permeability. (dovepress.com)
  • Viral vascular endothelial growth factors vary extensively in amino acid sequence, receptor-binding specificities, and the ability to induce vascular permeability yet are uniformly active mitogens. (smw.ch)
  • Takahashi H, Shibuya M. The vascular endothelial growth factor (VEGF)/VEGF receptor system and its role under physiological and pathological conditions. (smw.ch)
  • ABSTRACT We evaluated the prognostic value of serum endostatin and vascular endothelial growth factor (VEGF) for diagnosis of pre-eclampsia. (who.int)
  • Vascular endothelial growth factor (VEGF) plays a crucial role in physiological vasculogenesis and vascular permeability and has been implicated in the pathogenesis of pre-eclampsia. (who.int)
  • The data indicate that miR-210 is a key factor at the microRNA level in promoting angiogenesis and neurogenesis, which was associated with local increased vascular endothelial growth factor (VEGF) levels, suggesting that miR-210 may be a potential target for ischemic stroke therapy. (nih.gov)
  • Vascular endothelial growth factor (VEGF) blockade is an effective therapy for human cancer, yet virtually all neoplasms resume primary tumor growth or metastasize during therapy. (biomedcentral.com)
  • Combined treatment perturbed tumor vessel remodeling and macrophage recruitment, but did not further limit primary tumor growth as compared to VEGF blockade alone. (biomedcentral.com)
  • VEGF as an angiogenic growth factor and 20 weeks of pregnancy. (who.int)
  • Exosome uptake induced vascular endothelial growth factor (VEGF)-independent regulation of several angiogenesis-related genes, including von Willebrand factor, Tspan8, chemokines CXCL5 and MIF, chemokine receptor CCR1, and, together with VEGF, VEGF receptor 2. (unibas.ch)
  • The foremost regulator of angiogenesis is vascular endothelial growth factor (VEGF), which participates in the pathogenesis and progression of several cancers [ 9 ], and has been reported to be closely related to the clinical stages of OS [ 10 , 11 ]. (ijbs.com)
  • Interestingly, however, BIG1 and BIG2 knockdown significantly decreased the levels of VEGF mRNA and protein in glioblastoma U251 cells and HUVECs. (nih.gov)
  • The vitreous/serum ratio of the VEGF-A concentration in the PDR group (2.1 ± 1.8) was significantly higher compared with that in the control group (0.31 ± 0.33). (dovepress.com)
  • Similarly, VEGF-induced EC migration (2.5-fold) was significantly inhibited by EMAP II. (ikk-signaling.com)
  • With the help of chemically-modified small interfering RNAs targeting MALAT1 (siMALAT1), we confirm that siMALAT could provide a potential strategy to block the abnormally active OS-induced pro-angiogenic effect, and ultimately successfully suppress progression of OS tumours. (ijbs.com)
  • However, a more detailed and essential understanding of the countless ties between OS-induced angiogenesis and OS progression still requires further investigation. (ijbs.com)
  • In vivo studies designed to evaluate the impact of OCCs on the onset or progression of endometriosis and proliferation of induced endometriotic lesions were eligible. (nih.gov)
  • In addition, EMAP II inhibited binding of VEGF to VEGFR1 and VEGFR2. (ikk-signaling.com)
  • Hence, monoclonal antibodies against VEGF were introduced and used widely in the form of anti-VEGF agents, such as pegaptanib, ranibizumab, and bevacizumab. (dovepress.com)
  • The estrone-isoquinoline hybridized compound showed selective inhibitory activity against the proliferation and VEGF-induced migration of HUVEC. (go.jp)
  • Advanced lesions demonstrate a panarteritis with intimal proliferation. (medscape.com)
  • Given the role of multiple players during the pathogenesis of CNT-induced fibrosis, the objective of this review is to summarize the key findings and discuss major cellular and molecular events governing pulmonary fibrosis. (cdc.gov)
  • It regulates monocyte and macrophage migration, vascular permeability, haematopoiesis, and the recruitment of haematopietic progenitor cells from the bone marrow. (umbc.edu)
  • This study aimed to investigate the effects of se-methylselenocysteine (MSC) on oncogenesis of diethylnitrosamine (DEN)-induced hepatocellular carcinoma. (medscimonit.com)
  • The 'seeding' theory proposes that the formation of peritoneal dissemination is a multistep process, including detachment from the primary tumour, transmigration and attachment to the distant peritoneum, invasion into subperitoneal tissue and proliferation with blood vascular neogenesis. (spandidos-publications.com)
  • 2014). These pro-angiogenic elements accelerate the transition from 1 stage to a different through the angiogenesis approach, such as protease production, migration and proliferation of endothelial cells, vascular tube formation (canalization), anastomosis of newly formed vascular tubes, construction of a new basement membrane, and attachment of pericytes and smooth muscle cells (Rajabi and Mousa, 2017). (amparinhibitor.com)
  • 2005). Defensins also block VEGF-induced proliferation and VEGF- and bFGF-induced capillary formation potential of endothelial cells (Economopoulou et al. (amparinhibitor.com)
  • Protein array analysis showed upregulation of GM-CSF post anti-VEGF therapy. (nature.com)
  • The levels of VEGF are increased during infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), thus promoting inflammation by facilitating recruitment of inflammatory cells, and by increasing the level of angiopoietin II (Ang II), one of two products of the SARS-CoV-2 binding target, angiotensin-converting enzyme 2 (ACE2). (nih.gov)
  • In turn, Ang II facilitates the elevation of VEGF, thus forming a vicious cycle in the release of inflammatory cytokines. (nih.gov)