Evidence map›Paper›PMID 27115339›Full record

ArticleJournal of hypertension2016

Upregulation of P53 promoted G1 arrest and apoptosis in human umbilical cord vein endothelial cells from preeclampsia.

Qinqin Gao, Xiaolin Zhu, Jie Chen, Caiping Mao, Lubo Zhang, Zhice Xu

Abstract read
In one paragraph

Article in Journal of hypertension, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
6.7field-weighted citation impact, top 3% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. 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

6 authors at 1 institution in 1 country.

Qinqin GaoaInstitute for Fetology, The First Affiliated Hospital of Soochow University, Suzhou, China bCenter for Perinatal Biology, Loma Linda University, Loma Linda, California, USA *Qinqin Gao, Xiaolin Zhu and Jie Chen equally to this work.
Xiaolin Zhu
Jie Chen
Caiping Mao
Lubo Zhang
Zhice Xu
First Affiliated Hospital of Soochow University · CN

Funding

Uterine Vascular Adaptation to Pregnancy and Chronic HypoxiaP01HD083132 · NICHD · LOMA LINDA UNIVERSITY · PI DUCSAY, CHARLES A · 2016 to 2020
$6.3M
Epigenetic mechanisms of uterine vascular adaptation to pregnancy and hypoxiaR01HL128209 · NHLBI · LOMA LINDA UNIVERSITY · PI ZHANG, LUBO · 2015 to 2018
$1.6M
NHLBI NIH HHS R01 HL128209NICHD NIH HHS P01 HD083132
6 · The paper itself

Abstract

objectivePreeclampsia is a leading cause of maternal and perinatal morbidity and mortality. Current research has focused on endothelial dysfunction regarding pathogenesis of preeclampsia. However, very limited or no studies so far have been performed to assess possible damaged endothelial cell growth/development in the placenta-umbilical cord circulation system in human preeclampsia.

methodsWe isolated and cultured human umbilical cord vein endothelial cells (HUVECs) from normal and preeclampsia pregnancies in vitro. We used 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay to measure cell growth and flow cytometric analysis to determine cell-cycle distribution. Annexin V-fluorescein isothiocyanate/propidium iodide double staining was employed for cell apoptosis experiments.

resultsThe study showed that the cell growth was significantly suppressed, accompanied by the increased G1 arrest and apoptosis in cultured HUVECs from preeclampsia pregnancies comparing with normotensive controls. Protein P53 was upregulated in the cultured HUVECs from preeclampsia pregnancies, which induced G1 arrest, followed by upregulating P21 expression, and downregulating cyclin E expression and CDK2-cyclin E complexes. On the other hand, upregulation of P53 also activated Bax gene and repressed Bcl-2 and BIRC5 genes, resulting in an increase of the Bax/Bcl-2 ratio and subsequently activating caspase cascade, ultimately led to an initiation of the apoptotic machinery.

conclusionThese results indicated that in preeclampsia, vascular endothelial cells could be damaged and cellular proliferation was depressed in human placenta-umbilical cord circulation, adding new information on endothelial cell injury for better understanding the pathogenesis of preeclampsia.

Indexed as

AdultApoptosisbcl-2-Associated X ProteinCaspasesCell CycleCell ProliferationCells, CulturedCyclin-Dependent Kinase 2Cyclin-Dependent Kinase Inhibitor p21Cyclin EDown-RegulationFemaleG1 Phase Cell Cycle CheckpointsHumansHuman Umbilical Vein Endothelial CellsInhibitor of Apoptosis ProteinsBAX protein, humanbcl-2-Associated X ProteinBIRC5 protein, humanCaspasesCDKN1A protein, humanCyclin-Dependent Kinase 2Cyclin-Dependent Kinase Inhibitor p21Cyclin EInhibitor of Apoptosis ProteinsProto-Oncogene Proteins c-bcl-2RNA, MessengerSurvivinTumor Suppressor Protein p53

Identifiers

PMID27115339
PMCPMC5649442
OpenAlexW2344287365

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.