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VEGF (show VEGFA Proteins) and VEGFR1 levels in different regions of the normal and preeclampsia placentae.
High PlGF (show PGF Proteins) and/or low sFlt-1/PlGF (show PGF Proteins) may be used to diagnose Peripartum Cardiomyopathy.
Results demonstrate that short-activating RNA targeting the flt-1 promoter increased sFlt-1 mRNA and protein levels, while reducing VEGF expression. This was associated with suppression of human umbilical vascular endothelial cell (HUVEC) proliferation and cell cycle arrest at the G0/G1 phase. HUVEC migration and tube formation were also suppressed by Flt a-1.
In this context, our results demonstrate that D16F7 markedly inhibits chemotaxis and invasiveness of GBM cells and patient-derived GBM stem cells (GSCs) in response to VEGF-A (show VEGFA Proteins) and PlGF (show PGF Proteins), suggesting that VEGFR-1 might represent a suitable target that deserves further investigation for GBM treatment.
Study showed that term deliveries, higher soluble fms-like tyrosine kinase 1 (sFlt1) concentrations were associated with a smaller uterine artery resistance indices (RI) at the subsequent visit. For preterm delivery, higher sFlt1 concentrations were associated with a larger uterine artery RI.
Studied serum levels of soluble fms-like tyrosine kinase-1 (sFlt-1) and placental growth factor (PlGF (show PGF Proteins)) as markers for early diagnosis of preeclampsia.
This prospective observational study compare urine nephrin:creatinine ratio (NCR, ng/mg) with serum soluble fms-like tyrosine kinase-1:placental growth factor (show PGF Proteins) ratio (FPR (show FPR1 Proteins), pg/pg) for preeclampsia (PE) prediction among unselected asymptomatic pregnant women in 2(nd) trimester.
A high sFlt-1/PlGF (show PGF Proteins) ratio was associated with adverse outcomes and a shorter duration to delivery in early-onset fetal growth restriction.
Serum from type 2 diabetics reduced Akt (show AKT1 Proteins)/VEGFR-1 protein expression in endothelial progenitor cells.
The VEGF (show VEGFA Proteins)/sVEGF-R1 ratio in follicular fluid on the day of oocyte retrieval in women undergoing IVF (show SCN5A Proteins) procedure, regardless of the type of stimulation protocol, might predict the risk of developing ovarian hyperstimulation syndrome (OHSS). To the best of our knowledge this is the first paper in the literature to show interplay among VEGF (show VEGFA Proteins), EG-VEGF (show Prok1 Proteins) and sVEGF-R1 and the correlation between their concentration and OHSS risk.
we determined that radial glia control this process via the Vegf (show VEGFA Proteins) 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 (show AKT1 Proteins) pathway.
Elevated Notch (show NOTCH1 Proteins) signaling downstream of perturbed VEGF (show VEGFA Proteins) signaling contributes to aberrant flt-1(-/-) blood vessel formation.
Data indicate that the increase in FLT1/sFLT1 protein levels upon miR-10 (show LILRB2 Proteins) knockdown inhibited the angiogenic behavior of endothelial cells largely by antagonizing vascular endothelial growth factor receptor 2 (show KDR Proteins) signaling.
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 (show KDR Proteins) 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 (show PADI4 Proteins)(-/-) 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 (show KDR Proteins) 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.
These data therefore support a tightly controlled, paracrine signaling mechanism of VEGF-B (show VEGFB Proteins) to VEGFR1.
Flt1/VEGF-A (show VEGFA Proteins) signalling has stage-specific effects on vascular morphogenesis.
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 (show VEGFA Proteins) 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 (show VEGFA Proteins) and bFGF (show FGF2 Proteins) 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 (show TGFB1 Proteins) 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 (show KDR Proteins) heterodimer (VEGFR-1/R-2) is essential for PGI(2 (show PTGIR Proteins)) synthesis mediated by VEGF-A (show VEGFA Proteins)(165) and VEGF-A (show VEGFA Proteins)(121), which cannot be reproduced by the parallel activation of VEGFR-1 and VEGFR-2 (show KDR Proteins) homodimers with corresponding agonists
PEDF (show SERPINF1 Proteins) 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 (show KDR Proteins))in newborn piglet brain
data shows that members of the VEGF (show VEGFA Proteins)-VEGFR (show KDR Proteins) 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 (show EGFR Proteins), VEGFR (show KDR Proteins) and FGFR (show FGFR2 Proteins) are expressed in porcine oviduct and endometrium during the time of implantation [review]
VEGF (show VEGFA Proteins) ligand-receptor system may play an important role in the development and maintenance of the corpus luteum in pigs.
VEGF (show VEGFA Proteins)/Flk-1 (show KDR Proteins)/Flt-1 system is activated during myocardial ischemia reperfusion injury.
Hemodialysis graft placement leads to early increases in wall shear stress, VEGF-A (show VEGFA Proteins), pro-MMP-9 (show MMP9 Proteins), MMP-2 (show MMP2 Proteins), VEGFR-1, VEGFR-2 (show KDR Proteins), and TIMP-1 (show TIMP1 Proteins), which may contribute to the development of venous stenosis.
in experimental intervertebral disc degeneration, VEGF (show VEGFA Proteins) 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