Evidence map›Paper›PMID 31154903›Full record

ArticleHypertension (Dallas, Tex. : 1979)2019

Sexual Dimorphisms of Preeclampsia-Dysregulated Transcriptomic Profiles and Cell Function in Fetal Endothelial Cells.

Chi Zhou, Qin Yan, Qing-Yun Zou, Xin-Qi Zhong, Chanel T Tyler, Ronald R Magness, Ian M Bird, Jing Zheng

Open access · bronzeAbstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
9.0field-weighted citation impact, top 2% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
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  8. Prenatal exposure to environmentally relevant low-dosage dibutyl phthalate reduces placental efficiency in CD-1 mice.Toxicological sciences : an official journal of the Society of Toxicology · 2025
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  14. CaBiomedical reports · 2024
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  17. Fetal sexual dimorphism and preeclampsia among twin pregnancies.medRxiv : the preprint server for health sciences · 2023
    Article
  18. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 2 countries.

Chi ZhouFrom the Department of Obstetrics and Gynecology, University of Wisconsin-Madison (C.Z., Q.Y., Q.-Y.Z., X.-Q.Z., C.T.T., I.M.B., J.Z.).
Qin YanFrom the Department of Obstetrics and Gynecology, University of Wisconsin-Madison (C.Z., Q.Y., Q.-Y.Z., X.-Q.Z., C.T.T., I.M.B., J.Z.).
Qing-Yun ZouFrom the Department of Obstetrics and Gynecology, University of Wisconsin-Madison (C.Z., Q.Y., Q.-Y.Z., X.-Q.Z., C.T.T., I.M.B., J.Z.).
Xin-Qi ZhongFrom the Department of Obstetrics and Gynecology, University of Wisconsin-Madison (C.Z., Q.Y., Q.-Y.Z., X.-Q.Z., C.T.T., I.M.B., J.Z.).
Chanel T TylerFrom the Department of Obstetrics and Gynecology, University of Wisconsin-Madison (C.Z., Q.Y., Q.-Y.Z., X.-Q.Z., C.T.T., I.M.B., J.Z.).
Ronald R MagnessDepartment of Obstetrics and Gynecology, University of South Florida, Tampa (R.R.M.).
Ian M BirdFrom the Department of Obstetrics and Gynecology, University of Wisconsin-Madison (C.Z., Q.Y., Q.-Y.Z., X.-Q.Z., C.T.T., I.M.B., J.Z.).
Jing ZhengFrom the Department of Obstetrics and Gynecology, University of Wisconsin-Madison (C.Z., Q.Y., Q.-Y.Z., X.-Q.Z., C.T.T., I.M.B., J.Z.).
University of Wisconsin–Madison · USGuangdong Medical College · CNGuangzhou Medical University · CNShanghai First Maternity and Infant Hospital · CNUniversity of South Florida · US

Funding

Unified Cellular and Molecular CoreP01HD038843 · NICHD · UNIVERSITY OF WISCONSIN-MADISON · PI ZHENG, JING · 2001 to 2017
$14.4M
Endothelial Function in a Model of IUGR Induced by Uterine Space RestrictionR01HL117341 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI MAGNESS, RONALD R · 2014 to 2017
$1.8M
NHLBI NIH HHS R01 HL117341NICHD NIH HHS P01 HD038843
6 · The paper itself

Abstract

Preeclampsia impairs fetoplacental vascular function and increases risks of adult-onset cardiovascular disorders in children born to preeclamptic mothers, implicating that preeclampsia programs fetal vasculature in utero. However, the underlying mechanisms remain elusive. We hypothesize that preeclampsia alters fetal endothelial gene expression and disturbs cytokines- and growth factors-induced endothelial responses. RNA sequencing analysis was performed on unpassaged human umbilical vein endothelial cells (HUVECs) from normotensive and preeclamptic pregnancies. Functional assays for endothelial monolayer integrity, proliferation, and migration were conducted on passage 1 HUVECs from normotensive and preeclamptic pregnancies. Compared with normotensive cells, 926 and 172 genes were dysregulated in unpassaged female and male HUVECs from preeclamptic pregnancies, respectively. Many of these preeclampsia-dysregulated genes are associated with cardiovascular diseases (eg, heart failure) and endothelial function (eg, cell migration, calcium signaling, and endothelial nitric oxide synthase signaling). TNF (tumor necrosis factor)-α-, TGF (transforming growth factor)-β1-, FGF (fibroblast growth factor)-2-, and VEGFA (vascular endothelial growth factor A)-regulated gene networks were differentially disrupted in unpassaged female and male HUVECs from preeclamptic pregnancies. Moreover, preeclampsia decreased endothelial monolayer integrity in responses to TNF-α in both female and male HUVECs. Preeclampsia decreased TGF-β1-strengthened monolayer integrity in female HUVECs, whereas it enhanced FGF-2-strengthened monolayer integrity in male HUVECs. Preeclampsia promoted TNF-α-, TGF-β1-, and VEGFA-induced cell proliferation in female, but not in male HUVECs. Preeclampsia inhibited TNF-α-induced cell migration in female HUVECs, but had an opposite effect on male HUVECs. In conclusion, preeclampsia differentially dysregulates cardiovascular diseases- and endothelial function-associated genes/pathways in female and male fetal endothelial cells in association with the sexual dimorphisms of preeclampsia-dysregulated fetal endothelial function.

Indexed as

Sex CharacteristicsCells, CulturedDatabases, FactualFemaleGene Expression RegulationHumansHuman Umbilical Vein Endothelial CellsMalePre-EclampsiaPregnancyReal-Time Polymerase Chain ReactionSensitivity and SpecificitySignal TransductionStatistics, NonparametricTranscriptomeUp-RegulationVascular Endothelial Growth Factor Aendothelial dysfunctionhypertensionsex characteristicstranscriptomeumbilical veins

Identifiers

PMID31154903
PMCPMC6561818
OpenAlexW2948939913

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.