Evidence map›Paper›PMID 30316329›Full record

ArticlePlacenta2018

FMS-like tyrosine kinase 1 (FLT1) is a key regulator of fetoplacental endothelial cell migration and angiogenesis.

Shuhan Ji, Hong Xin, Yingchun Li, Emily J Su

Open access · greenAbstract read
In one paragraph

Article in Placenta, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.1field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 31 citations in OpenAlex.

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  7. Bioinformatics analysis explores key pathways and hub genes in central precocious puberty.Journal of pediatric endocrinology & metabolism : JPEM · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Shuhan JiDivision of Reproductive Sciences, University of Colorado School of Medicine, Aurora, CO, USA.
Hong XinDivision of Reproductive Sciences, University of Colorado School of Medicine, Aurora, CO, USA.
Yingchun LiDivision of Reproductive Sciences, University of Colorado School of Medicine, Aurora, CO, USA.
Emily J SuDivision of Reproductive Sciences, University of Colorado School of Medicine, Aurora, CO, USA; Division of Maternal-Fetal Medicine, University of Colorado School of Medicine, Aurora, CO, USA. Electronic address: Emily.su@ucdenver.edu.
University of Colorado Denver · US

Funding

University of Colorado Cancer Center Support Grant - Lung Cancer Patient-Derived Xenografts with Autologous Human Immune SystemsP30CA046934 · NCI · UNIVERSITY OF COLORADO DENVER · PI James V Degregori · 1988 to 2026
$117.0M
Mediators of impaired fetoplacental angiogenesis in fetal growth restrictionR01HL119846 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI SU, EMILY J · 2014 to 2023
$4.9M
NCI NIH HHS P30 CA046934NHLBI NIH HHS R01 HL119846
6 · The paper itself

Abstract

introductionFetoplacental angiogenesis plays a vital role in pregnancy outcome. Vascular endothelial growth factor A (VEGFA) is one major regulator of angiogenesis. It primarily binds to FMS-like tyrosine kinase (FLT1) and kinase insert domain receptor (KDR). In most vascular beds, KDR appears to be the main mediator of angiogenesis. However, the role of both receptors within the human placenta remains unknown.

methodsHuman fetoplacental ECs were isolated/cultured from placentas of full-term, uncomplicated pregnancies after scheduled Cesarean section. Cells were subjected to RNA interference of either FLT1 or KDR followed by MTT, wound scratch, and tube formation assays. ECs were serum-starved after RNA interference and treated with VEGFA (60 ng/ml), then subjected to western blot to investigate FLT1 or KDR-mediated signaling. All experiments were performed in triplicate utilizing ECs from at least three separate subjects. One-way ANOVA with Tukey post-hoc testing was utilized for statistical analysis.

resultsSignificant knock-down of FLT1 and KDR was confirmed by qPCR (p < 0.01) and WB (p < 0.0001). KDR knock-down decreased EC metabolic activity (p < 0.01), and FLT1 ablation unexpectedly increased EC proliferation (p < 0.01). There was no difference in apoptosis regardless of FLT-1 or KDR knock-down. FLT1 knock-down significantly impaired wound scratch closure (p < 0.0001) and tube formation (p < 0.001). Surprisingly, KDR effects on EC metabolism had no effect on migration, although KDR was important in VEGFA-stimulated Akt and ERK activation. In contrast, FLT1 effects on EC motility were Akt and ERK-independent.

conclusionHuman fetoplacental EC migration is primarily regulated by FLT1 but not KDR.

Indexed as

ApoptosisCell MovementCell ProliferationEndothelial CellsEndothelium, VascularFemaleHumansNeovascularization, PhysiologicPlacentaPregnancySignal TransductionVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth Factor Receptor-2FLT1 protein, humanVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth Factor Receptor-2Endothelial migrationFLT1Human fetoplacental endothelial cellsKDR

Identifiers

PMID30316329
PMCPMC6342273
OpenAlexW2888358999

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.