Evidence map›Paper›PMID 28986273›Full record

ArticleReproductive toxicology (Elmsford, N.Y.)2017

ITE Suppresses Angiogenic Responses in Human Artery and Vein Endothelial Cells: Differential Roles of AhR.

Yan Li, Kai Wang, Qing-Yun Zou, Yi-Zhou Jiang, Chi Zhou, Jing Zheng

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Reproductive toxicology (Elmsford, N.Y.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 27% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 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

6 authors at 1 institution in 2 countries.

Yan LiDepartment of Obstetrics and Gynecology, University of Wisconsin-Madison, Madison, WI 53715, United States.
Kai WangDepartment of Obstetrics and Gynecology, University of Wisconsin-Madison, Madison, WI 53715, United States.
Qing-Yun ZouDepartment of Obstetrics and Gynecology, University of Wisconsin-Madison, Madison, WI 53715, United States.
Yi-Zhou JiangDepartment of Obstetrics and Gynecology, University of Wisconsin-Madison, Madison, WI 53715, United States.
Chi ZhouDepartment of Obstetrics and Gynecology, University of Wisconsin-Madison, Madison, WI 53715, United States.
Jing ZhengDepartment of Obstetrics and Gynecology, University of Wisconsin-Madison, Madison, WI 53715, United States; Cardiovascular Medicine Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang 524001, Guangdong, China. Electronic address: jzheng@wisc.edu.
University of Wisconsin–Madison · US

Funding

Unified Cellular and Molecular CoreP01HD038843 · NICHD · UNIVERSITY OF WISCONSIN-MADISON · PI ZHENG, JING · 2001 to 2017
$14.4M
Epigenetic regulation of endothelial phenotype by flow and hypercholesterolemia in vivo and in vitroK99HL127272 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI JIANG, YIZHOU · 2016 to 2017
$216k
NHLBI NIH HHS K99 HL127272NICHD NIH HHS P01 HD038843
6 · The paper itself

Abstract

Aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor is involved in regulation of many essential biological processes including vascular development and angiogenesis. 2-(1'H-indole-3'-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE) is an AhR ligand, which regulates immune responses and cancer cell growth. However, the roles of the ITE/AhR pathway in mediating placental angiogenesis remains elusive. Here, we determined if ITE affected placental angiogenic responses via AhR in human umbilical vein (HUVECs) and artery endothelial (HUAECs) cells in vitro. We observed that ITE dose- and time-dependently inhibited proliferation and viability of HUAECs and HUVECs, whereas it inhibited migration of HUAECs, but not HUVECs. While AhR siRNA significantly suppressed AhR protein expression in HUVECs and HUAECs, it attenuated the ITE-inhibited angiogenic responses of HUAECs, but not HUVECs. Collectively, ITE suppressed angiogenic responses of HUAECs and HUVECs, dependent and independent of AhR, respectively. These data suggest that ITE may regulate placental angiogenesis.

Indexed as

Cell MovementCell ProliferationCells, CulturedCell SurvivalCytochrome P-450 CYP1A1Cytochrome P-450 CYP1B1Endothelial CellsHumansIndolesNeovascularization, PhysiologicNeuropilin-1Receptors, Aryl HydrocarbonThiazolesUmbilical ArteriesUmbilical Veins2-(1'H-indole-3'-carbonyl)thiazole-4-carboxylic acid methyl esterCYP1A1 protein, humanCYP1B1 protein, humanCytochrome P-450 CYP1A1Cytochrome P-450 CYP1B1IndolesNeuropilin-1Receptors, Aryl HydrocarbonThiazolesAngiogenesisAryl hydrocarbon receptorEndothelial cellsITE

Identifiers

PMID28986273
PMCPMC5718942
OpenAlexW2762204972

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.