Evidence map›Paper›PMID 32003123›Full record

ArticleJournal of cellular and molecular medicine2020

Down-regulation of endothelial protein C receptor promotes preeclampsia by affecting actin polymerization.

Hao Wang, Pan Wang, Xiaoling Liang, Wenjing Li, Mo Yang, Jihong Ma, Wei Yue, Shangrong Fan

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 23% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Knowledge-Driven Mechanistic Enrichment of the Preeclampsia Ignorome.Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing · 2023
    Pooled it
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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

8 authors at 4 institutions in 1 country.

Hao WangDepartment of Obstetrics and Gynecology, Peking University Shenzhen Hospital, Shenzhen, China.ORCID 0000-0001-6441-0453
Pan WangDepartment of Obstetrics and Gynecology, Peking University Third Hospital, Beijing, China.
Xiaoling LiangDepartment of Obstetrics and Gynecology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Wenjing LiDepartment of Obstetrics and Gynecology, Peking University Third Hospital, Beijing, China.
Mo YangMedical Center for Human Reproduction, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Jihong MaDepartment of Obstetrics and Gynecology, Peking University Third Hospital, Beijing, China.
Wei YueDepartment of Obstetrics and Gynecology, Peking University Third Hospital, Beijing, China.
Shangrong FanDepartment of Obstetrics and Gynecology, Peking University Shenzhen Hospital, Shenzhen, China.
Peking University · CNPeking University Shenzhen Hospital · CNCapital Medical University · CNSir Run Run Shaw Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Preeclampsia is a severe pregnancy-related disease that is found in 3%-5% of pregnancies worldwide and is primarily related to the decreased proliferation and invasion of trophoblast cells and abnormal uterine spiral artery remodelling. However, studies on the pathogenesis of placental trophoblasts are insufficient, and the aetiology of PE remains unclear. Here, we report that endothelial protein C receptor (EPCR), a transmembrane glycoprotein, was down-regulated in placentas from preeclamptic patients. Moreover, lack of EPCR significantly reduced the trophoblast cell proliferation, invasion and tube formation capabilities. Microscale thermophoresis analysis showed that EPCR directly bound to protease-activated receptor 1 (PAR-1), a G protein-coupled receptor. This change resulted in a substantial reduction in active Rac1 and caused excessive actin rearrangement. Our findings reveal a previously unidentified role of EPCR in the regulation of trophoblast proliferation, invasion and tube formation through promotion of actin polymerization, which is required for normal placental development.

Indexed as

ActinsAdultCell LineCell ProliferationCRISPR-Cas SystemsDown-RegulationEndothelial Protein C ReceptorFemaleGene Knockout TechniquesHumansHypertensionPlacentaPre-EclampsiaPregnancyPregnancy ComplicationsProtein Serine-Threonine KinasesActinsEndothelial Protein C ReceptorMARK2 protein, humanPROCR protein, humanProtein Serine-Threonine Kinasesrac1 GTP-Binding ProteinRAC1 protein, humancell invasioncell proliferationendothelial protein C receptorpreeclampsiatube formation

Identifiers

PMID32003123
PMCPMC7131931
OpenAlexW3004248572

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.