Evidence map›Paper›PMID 26275813›Full record

ArticleToxicology2015

2,3,7,8-Tetrachlorodibenzo-p-dioxin differentially suppresses angiogenic responses in human placental vein and artery endothelial cells.

Yan Li, Kai Wang, Qing-Yun Zou, Ronald R Magness, Jing Zheng

Abstract read
In one paragraph

Article in Toxicology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
13.8field-weighted citation impact, top 1% 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

22 citing papers in PubMed, 42 citations in OpenAlex.

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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

5 authors at 3 institutions in 2 countries.

Yan LiDepartment of Obstetrics and Gynecology, Perinatal Research Laboratories, University of Wisconsin-Madison, Madison, WI 53715, USA.
Kai WangShanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai 200040, PR China.
Qing-Yun ZouDepartment of Obstetrics and Gynecology, Perinatal Research Laboratories, University of Wisconsin-Madison, Madison, WI 53715, USA.
Ronald R MagnessDepartment of Obstetrics and Gynecology, Perinatal Research Laboratories, University of Wisconsin-Madison, Madison, WI 53715, USA; Departments of Pediatrics, University of Wisconsin-Madison, Madison, WI 53715, USA; Department of Animal Sciences, University of Wisconsin-Madison, Madison, WI 53715, USA.
Jing ZhengDepartment of Obstetrics and Gynecology, Perinatal Research Laboratories, University of Wisconsin-Madison, Madison, WI 53715, USA; Department of Cardiovascular Medicine, Affiliated Hospital of Guangdong Medical College, Zhanjiang 524001, Guangdong, PR China. Electronic address: jzheng@wisc.edu.
University of Wisconsin–Madison · USGuangdong Medical College · CNShanghai First Maternity and Infant Hospital · CN

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 HD38843NICHD NIH HHS P01 HD038843
6 · The paper itself

Abstract

Placental angiogenesis is dramatically increased during pregnancy in association with the elevated placental blood flows to support the rapidly growing fetus. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is an environmental toxicant and a ligand of aryl hydrocarbon receptor (AhR). Herein, we investigated the effects of TCDD on proliferation, migration, and viability of fetoplacental endothelial cells in response to a complete growth medium which contained serum and growth supplement using human umbilical cord vein (HUVECs) and artery (HUAECs) cells as models. We found that TCDD dose- and time-dependently inhibited (p < 0.05) proliferation of HUVECs and HUAECs. Treatment with TCDD at 10 nM for 6 days inhibited (p < 0.05) migration (by ∼ 30%) of HUAECs, but not HUVECs. TCDD at 10nM also decreased (p < 0.05) viability of HUVECs and HUAECs. Interestingly, specific AhR siRNA blocked (p < 0.05) the TCDD-inhibited cellular responses in HUAECs, but not HUVECs. Nonetheless, TCDD at 10nM neither affected the cell cycle progression, nor did it induce cell apoptosis in HUVECs and HUAECs. In addition, TCDD at 10 nM also did not alter activation of ERK1/2 and AKT1 in HUVECs and HUAECs. Collectively, TCDD suppresses proliferation and/or migration (two key steps of angiogenesis) of HUVECs and HUAECs independent and dependent of AhR, respectively. These data suggest that TCDD inhibited growth of HUVECs and HUAECs via decreasing cell viability. Thus, TCDD may inhibit fetoplacental angiogenesis, leading to negative pregnancy outcomes.

Indexed as

Cell CycleCell ProliferationCells, CulturedCell SurvivalDose-Response Relationship, DrugEndothelium, VascularFemaleHumansNeovascularization, PhysiologicPlacentaPolychlorinated DibenzodioxinsPregnancyUmbilical ArteriesUmbilical VeinsPolychlorinated DibenzodioxinsAngiogenesisAryl hydrocarbon receptorEndothelial cellsPlacentaTCDD

Identifiers

PMID26275813
PMCPMC4593512
OpenAlexW1175945741

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.