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A single measurement of sFlt-1/PlGF (显示 PGF 蛋白) ratio at third trimester to predict pre-eclampsia and intrauterine growth retardation occurring after 34weeks of pregnancy.
sFlt1 was produced in significant amounts by preeclamptic peripheral blood mononuclear leukocytes, and ex vivo studies show that the placenta induces this over-expression. In contrast, exposure to PBMCs appears to decrease sFlt1 production by preeclamptic placenta.
The levels of sFlt-1, PlGF (显示 PGF 蛋白), and the sFlt-1/PlGF (显示 PGF 蛋白) ratio in pre-eclamptic women with an onset at < 32 weeks were sig (显示 PICALM 蛋白)- ni fi cantly di ff erent from those in women with an onset at >/=32-33 weeks.
These results showed that arginase controlled sFlt-1 elevation to some extent.
These results suggest that VM formation is increased by EBVLMP1 via VEGF (显示 VEGFA 蛋白)/VEGFR1 signaling and provide additional information to clarify the role of EBVLMP1 in nasopharyngeal carcinoma (NPC (显示 NPC1 蛋白))pathophysiology
An sFlt-1:PlGF (显示 PGF 蛋白) ratio above 655 is not predictive of impaired perinatal outcomes, and insufficiently reliable for predicting outcomes in cases with clinical signs of preeclampsia.
The maternal sFlt-1 to PlGF (显示 PGF 蛋白) ratio in women with hypertensive disorders in pregnancy carries prognostic value for the development of preeclampsia.
VEGFA (显示 VEGFA 蛋白) activates VEGFR1 homodimers and AKT (显示 AKT1 蛋白), leading to a cytoprotective response, whilst abluminal VEGFA (显示 VEGFA 蛋白) induces vascular leakage via VEGFR2 (显示 KDR 蛋白) homodimers and p38 (显示 CRK 蛋白)
metformin's dual effect in hyperglycemia-chemical hypoxia is mediated by direct effect on VEGFR1/R2 leading to activation of cell migration through MMP16 (显示 MMP16 蛋白) and ROCK1 (显示 ROCK1 蛋白) upregulation, and inhibition of apoptosis by increase in phospho-ERK1/2 and FABP4 (显示 FABP4 蛋白), components of VEGF (显示 VEGFA 蛋白) signaling cascades
Additionally, LVsFlt1MSCs inhibited tumor growth and prolonged survival in an hepatocellular carcinoma (HCC (显示 FAM126A 蛋白))mouse model via systemic injection. Overall, the present study was designed to investigate the potential of LVsFlt1MSCs for antiangiogenesis gene therapy in HCC (显示 FAM126A 蛋白).
we determined that radial glia control this process via the Vegf (显示 VEGFA 蛋白) decoy receptor sFlt1: sflt1 mutants exhibit the venous over-sprouting observed in radial glia-ablated larvae, and sFlt1 overexpression rescues it. Genetic mosaic analyses show that sFlt1 function in trunk endothelial cells can limit their over-sprouting.
Flt1-tyrosine kinase (TK) activity contributed significantly in endothelial cells survival and vascular development during embryo angiogenesis in zebrafish by engaging PI3K/Akt (显示 AKT1 蛋白) pathway.
Elevated Notch (显示 NOTCH1 蛋白) signaling downstream of perturbed VEGF (显示 VEGFA 蛋白) signaling contributes to aberrant flt-1(-/-) blood vessel formation.
Data indicate that the increase in FLT1/sFLT1 protein levels upon miR-10 (显示 LILRB2 蛋白) knockdown inhibited the angiogenic behavior of endothelial cells largely by antagonizing vascular endothelial growth factor receptor 2 (显示 KDR 蛋白) signaling.
inducible endothelial genetic deletion of Neuropilin1 (Nrp1 (显示 NRP1 蛋白)) and Vascular endothelial growth factor receptor 1 (Vegfr1; also known as Flt1) renders mice resistant to diet-induced obesity.
findings identified a novel function of the VEGFR1 signaling in avoiding over-expression of Arginase 1 (显示 ARG1 蛋白) potentially to maintain the proper innate immune response.
Results show that Flt1 heterozygosity causes embryonic edema with enhanced vascular permeability. It can also be a risk factor for embryonic lethality in combination with other mutations causing non-lethal vascular phenotype.
Our study suggests that "migration" of the placenta is derived from placental degeneration at the caudal part of the placenta, and sFlt-1 plays a role in this placental degeneration.
This is the first report demonstrating the spatiotemporal expression patterns of Flk1 (显示 KDR 蛋白) and Flt1 in the coronary vascular system during development and after MI; thus, this study suggests that these factors have distinct and important functions in coronary angiogenesis.
sFlt-1 overexpression in Padi4 (显示 PADI4 蛋白)(-/-) mice resulted in dramatically lower inflammatory and thrombotic response, which was accompanied by significant reduction in pregnancy losses. Inhibition of NETosis may serve as a novel target in disorders of impaired placentation.
endothelial dysfunction due to high circulating sFLT1 may be the primary event leading to enhanced vasoconstrictor sensitivity that is characteristic of preeclampsia
Flt1 has a role in blood vessel anastomosis during angiogenesis
First-in-class selective PET tracers for imaging VEGFR-1 and VEGFR-2 (显示 KDR 蛋白) were constructed and successfully validated in an orthotopic murine tumor model.
these results suggest that VEGFR1 signaling plays a role in regulating the balance between macrophage phenotypes in streptozotocin -induced diabetic wounds, prevents impaired diabetic wound healing, and promotes angiogenesis/lymphangiogenesis.
There is a possibility that steatosis can be suppressed by the CC genotype in VEGFR1.
These results suggest that non-dominant follicles maintain a greater concentration of the mRNA expression of both membrane and soluble VEGF (显示 VEGFA 蛋白) receptors; but follicular dominance is related to a reduction in the mRNA expression of sVEGFR1 and sVEGFR2.
VEGFR-1 negatively regulates primary bovine retinal pericytes survival, and its blockade protects the blood-brain barrier integrity.
gamma-Secretase and presenilin mediate cleavage and phosphorylation of vascular endothelial growth factor receptor-1
VEGFR1 mRNA expression was lower at estrus and at the early I and early II luteal stages than at the other stages, whereas VEGFR1 protein expression did not change significantly throughout the estrous cycle (P<0.05)
Alterations in the expression of VEGF-A (显示 VEGFA 蛋白) and bFGF (显示 FGF2 蛋白) systems suggest that angiogenic factors are involved in abnormal placental development in cloned gestations, contributing to impaired fetal development and poor survival rates.
inhibition of VEGFR-1 results in decrease in number of capillary connections indicating VEGFR-1 ligands promote branching angiogenesis.
TGF-beta1 (显示 TGFB1 蛋白) induction of VEGFR-1 in endothelial cells explains pericyte protection of vessels and the selective vulnerability of neonatal vessels to oxygen(VEGFR-1)
the activation of VEGFR-1 and VEGFR-2 (显示 KDR 蛋白) heterodimer (VEGFR-1/R-2) is essential for PGI(2 (显示 PTGIR 蛋白)) synthesis mediated by VEGF-A (显示 VEGFA 蛋白)(165) and VEGF-A (显示 VEGFA 蛋白)(121), which cannot be reproduced by the parallel activation of VEGFR-1 and VEGFR-2 (显示 KDR 蛋白) homodimers with corresponding agonists
PEDF (显示 SERPINF1 蛋白) and VEGFR-1 have roles in the negative regulation of angiogenesis
FLT-1 differentially methylated region was hypermethylated in parthenogenetic placenta.
we analyzed the expression and cellular distribution of Flt-1(VEGFR-1) and Flk-1 (KDR/VEGFR-2 (显示 KDR 蛋白))in newborn piglet brain
data shows that members of the VEGF (显示 VEGFA 蛋白)-VEGFR (显示 KDR 蛋白) system are temporally and spatially well localized for playing key roles during umbilical cord formation and its intensive growth observed after day 75 of pregnancy
The VEGFR1 was stably expressed during the whole lifespan of mesonephric glomeruli, and VEGFR1 is important for the maintenance of endothelial fenestrations.
increased placental expression of the VEGF receptor system is associated with increased placental vascular density observed with the advancement of gestation in the pig.
EGFR (显示 EGFR 蛋白), VEGFR (显示 KDR 蛋白) and FGFR (显示 FGFR2 蛋白) are expressed in porcine oviduct and endometrium during the time of implantation [review]
VEGF (显示 VEGFA 蛋白) ligand-receptor system may play an important role in the development and maintenance of the corpus luteum in pigs.
VEGF (显示 VEGFA 蛋白)/Flk-1 (显示 KDR 蛋白)/Flt-1 system is activated during myocardial ischemia reperfusion injury.
Hemodialysis graft placement leads to early increases in wall shear stress, VEGF-A (显示 VEGFA 蛋白), pro-MMP-9 (显示 MMP9 蛋白), MMP-2 (显示 MMP2 蛋白), VEGFR-1, VEGFR-2 (显示 KDR 蛋白), and TIMP-1 (显示 TIMP1 蛋白), which may contribute to the development of venous stenosis.
in experimental intervertebral disc degeneration, VEGF (显示 VEGFA 蛋白) receptors were expressed in the damaged disc and paradiscal tissues
This gene encodes a member of the vascular endothelial growth factor receptor (VEGFR) family. VEGFR family members are receptor tyrosine kinases (RTKs) which contain an extracellular ligand-binding region with seven immunoglobulin (Ig)-like domains, a transmembrane segment, and a tyrosine kinase (TK) domain within the cytoplasmic domain. This protein binds to VEGFR-A, VEGFR-B and placental growth factor and plays an important role in angiogenesis and vasculogenesis. Expression of this receptor is found in vascular endothelial cells, placental trophoblast cells and peripheral blood monocytes. Multiple transcript variants encoding different isoforms have been found for this gene. Isoforms include a full-length transmembrane receptor isoform and shortened, soluble isoforms. The soluble isoforms are associated with the onset of pre-eclampsia.
fms-like tyrosine kinase 1
, fms-related tyrosine kinase 1 (vascular endothelial growth factor/vascular permeability factor receptor)
, tyrosine-protein kinase FRT
, tyrosine-protein kinase receptor FLT
, vascular endothelial growth factor receptor 1
, vascular permeability factor receptor
, FMS-like tyrosine kinase 1
, Fms-related tyrosine kinase 1 (vascular endothelial growth factor/vascular permeability factor receptor)
, vascular endothelial growth factor receptor-1
, fms-related tyrosine kinase 1
, receptor tyrosine kinase Flt1b
, soluble fms-like tyrosine kinase 1
, embryonic receptor kinase 2
, vascular endothelial growth factor/vascular permeability factor receptor
, ascular endothelial growth factor/vascular permeability factor receptor
, vascular endothelial growth factor 1
, flt-1 type VEGF receptor