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Rat (Rattus) PGF Protein expressed in Escherichia coli (E. coli) - ABIN2126310
Zhang, Zhao, Yuan, Wu, Jiang, Luo, Zhao: Knockdown of placental growth factor (PLGF) mitigates hyperoxia-induced acute lung injury in neonatal rats: Suppressive effects on NFκB signaling pathway. in International immunopharmacology 2016
Human PGF Protein expressed in Escherichia coli (E. coli) - ABIN413725
Ding, Huang, Song, Gao, Yuan, Wang, Cai, Fu, Luo: NFAT1 mediates placental growth factor-induced myelomonocytic cell recruitment via the induction of TNF-alpha. in Journal of immunology (Baltimore, Md. : 1950) 2010
low serum level associated with stillbirth
sFlt-1/PLGF was positively correlated with the severity of preterm preeclampsia.
The relationship between PlGF and preeclampsia differed in women with obesity according to gestational diabetes status, which may suggest different mechanistic pathways to preeclampsia.
A contingent strategy of measuring the sFlt-1/PlGF ratio at 24-28weeks in women previously selected by clinical factors and uterine artery Doppler enables an accurate prediction of preeclampsia/fetal growth restriction.
modest correlation of serum-free PlGF-1 with placental volume and uterine artery Doppler pulsatility index
PGF promotes epithelial-mesenchymal transition-like changes in retinal pigment epithelium cells under hypoxia by activating the NF-kappaB signaling pathway.
PGF expression may have a role in lymphatic invasion, poorer response to chemotherapy and unfavorable prognosis of patients with serous epithelial ovarian cancer
A single measurement of sFlt-1/PlGF ratio at third trimester to predict pre-eclampsia and intrauterine growth retardation occurring after 34weeks of pregnancy.
The levels of sFlt-1, PlGF, and the sFlt-1/PlGF ratio in pre-eclamptic women with an onset at < 32 weeks were sig- ni fi cantly di ff erent from those in women with an onset at >/=32-33 weeks.
In urban Mozambican women with symptoms and/or signs suggestive of preeclampsia, low maternal plasma PlGF concentrations are associated with increased risks of adverse pregnancy outcomes, especially early delivery and stillbirth.
An sFlt-1:PlGF 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 ratio in women with hypertensive disorders in pregnancy carries prognostic value for the development of preeclampsia.
Data suggest that PGF and PAPPA serve as serum biomarkers for early diagnosis of gestational hypertension. These studies were conducted at antenatal clinics in Ghana using blood from women between 8 and 13 weeks gestation. (PGF = placental growth factor; PAPPA = pregnancy-associated plasma protein-A)
Lower umbilical cord PlGF levels are associated with lower birth weight, deviating fetal growth patterns, and a higher odds of fetal growth retardation.
Data suggest that circulating PGF levels fall by nearly one quarter during term labor (but not during elective caesarean section).
The cross-talk between tumor-associated macrophages and NSCLC cells via PLGF/Flt-1 and TGFbeta receptor signaling may promote the growth and vascularization of NSCLC.
PlGF level showed an inversely proportional effect on the foetal weight.
Recombinant hPlGF-2 significantly improved contractile function and reduced LV end-systolic and end-diastolic volume indices with a concomitant increase in capillary and arteriolar density in ischemic myocardium, without aggravating atherosclerosis.
these data suggest that PlGF may increase non-small cell lung cancer metastasis through SRp40-mediated mRNA splicing of VEGF.
The present study investigated the interplay of VEGF-A165a isoform, the anti-angiogenic VEGF-A165b, placental growth factor (PIGF) and their receptors, VEGFR1 and VEGFR2, on junctional occupancy of VE-cadherin and macromolecular leakage in human endothelial monolayers and the perfused placental microvascular bed.
Common bile duct ligation in mice induces hepatopulmonary syndrome , which is mediated by PlGF production; alphaPlGF treatment improves experimental hepatopulmonary syndrome by counteracting pulmonary angiogenesis and might be an attractive therapeutic strategy for human hepatopulmonary syndrome
elevated PlGF levels may contribute to recruitment and activation of leukocytes. This can subsequently lead to increased pathology of affected organs in addition to mediating acute hypoxia/reoxygenation-triggered vaso-occlusion under sickle cell disease conditions.
Data indicate that VEGF-B is a high-affinity VEGFR-1 ligand that, unlike PIGF, cannot efficiently induce signaling downstream of VEGFR-1.
the lack of PIGF may have contributed to the delayed angiogenic response and the prothrombotic phenotype observed in the PIGF(-/-)animals.
Overexpression of VEGF but not PIGF exacerbated the lipopolysaccharide-mediated toxic effects, supporting a pathophysiological role for VEGF in mediating the sepsis phenotype.
Findings indicate that placental growth factor (PlGF) plays an important role in liver fibrosis-associated angiogenesis and that blockage of PlGF could be an effective strategy for chronic liver disease.
Data demonstrate that PlGF is expressed in vivo and that its expression is restricted to the areas of the tumors where the highest levels of hypoxia occur. Also, hypoxia activates PlGF expression in cultured lymphatic endothelial cells.
Study provides mechanistic and clinical evidence that decreased PLGF levels in the placenta after in utero alcohol exposure are associated to brain angiogenesis defects. Measurement of PLGF levels at birth in the placenta or the fetal blood may serve as a predictive marker for subsequent neurodevelopmental outcomes of exposed fetuses.
PGF deficiency is associated with impaired cerebral vascular development in mice.
PlGF inhibition attenuates PERK activation, likely by tempering hypoxia in HCC via vessel normalisation. The UPR is able to regulate PlGF expression, suggesting the existence of a feedback mechanism for hypoxia-mediated UPR
Placenta growth factor augments airway hyperresponsiveness via leukotrienes and IL-13.
Data indicate that placental growth factor (PlGF) is needed in the spleen to allow the activation of T cells and blood pressure raising.
Placental growth factor promotes differentiation of bone marrow-derived macrophages and enhanced vascular endothelial cell proliferation.
PLGF in LC cells induced macrophage polarization in vivo, and significantly promoted the growth of LC.
PLGF is upregulated in vascular cells in response to fluid shear stress.
Data suggests that PLGF may target islet endothelia to release growth factors activating PI3k signalling in beta cells to increase their proliferation. In Pre-Eclampsia, PLGF reduction impairs these processes resulting in gestational diabetes mellitus.
The neutrophil elastase-PlGF-JNK/PKCdelta pathway contributes to the pathogenesis of lung epithelial cell apoptosis and emphysema.
E2F1 limits cardiac neovascularization and functional recovery after myocardial infarction by suppressing VEGF and PlGF up-regulation through p53-dependent and -independent mechanisms, respectively.
Pgf knockout mice had higher systolic blood pressure in early and late pregnancy but an extended, abnormal midpregnancy interval of depressed systolic pressure. Knockout kidneys were hypertrophic and had glomerular pathology.
PLGF triggers focal adhesion disassembly in alveolar type II cells via inhibiting the activation of focal adhesion kinase.
Study reports polymorphisms in the bovine PGF gene significantly associated with the maternal effect on stillbirth and calving ease in animals under selection.
placenta growth factor expression is regulated by both VEGF and hyperglycaemia via VEGFR-2
This gene encodes a growth factor found in placenta which is homologous to vascular endothelial growth factor. Alternatively spliced transcripts encoding different isoforms have been found for this gene.
placenta growth factor
, placental growth factor, vascular endothelial growth factor-related protein
, placenta growth factor-like