Evidence map›Paper›PMID 28699682›Full record

ArticleJournal of cellular and molecular medicine2017

2, 3, 7, 8-Tetrachlorodibenzo-p-dioxin promotes endothelial cell apoptosis through activation of EP3/p38MAPK/Bcl-2 pathway.

Yu Yu, Qian Liu, Shumin Guo, Qianqian Zhang, Juan Tang, Guizhu Liu, Deping Kong, Juanjuan Li, Shuai Yan, Ruiguo Wang and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 29 citations in OpenAlex.

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  8. Review
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  11. 2,3,7,8-Tetrachlorodibenzo-BioMed research international · 2020
    Article
  12. Review
  13. Article
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  15. Article
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

13 authors at 3 institutions in 1 country.

Yu YuDepartment of Pharmacology, Tianjin Medical University, Tianjin, China.
Qian LiuDepartment of Pharmacology, Tianjin Medical University, Tianjin, China.
Shumin GuoDepartment of Pharmacology, Tianjin Medical University, Tianjin, China.
Qianqian ZhangKey Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Juan TangKey Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Guizhu LiuKey Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Deping KongDepartment of Pharmacology, Tianjin Medical University, Tianjin, China.
Juanjuan LiKey Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Shuai YanKey Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Ruiguo WangInstitute of Quality Standards and Testing Technology for Agro-products, Chinese Academy of Agricultural Sciences, Beijing, China.
Peilong WangInstitute of Quality Standards and Testing Technology for Agro-products, Chinese Academy of Agricultural Sciences, Beijing, China.
Xiaoou SuInstitute of Quality Standards and Testing Technology for Agro-products, Chinese Academy of Agricultural Sciences, Beijing, China.
Ying YuDepartment of Pharmacology, Tianjin Medical University, Tianjin, China.ORCID http://orcid.org/0000-0003-2427-0411
Chinese Academy of Sciences · CNChinese Academy of Agricultural Sciences · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial injury or dysfunction is an early event in the pathogenesis of atherosclerosis. Epidemiological and animal studies have shown that 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD) exposure increases morbidity and mortality from chronic cardiovascular diseases, including atherosclerosis. However, whether or how TCDD exposure causes endothelial injury or dysfunction remains largely unknown. Cultured human umbilical vein endothelial cells (HUVECs) were exposed to different doses of TCDD, and cell apoptosis was examined. We found that TCDD treatment increased caspase 3 activity and apoptosis in HUVECs in a dose-dependent manner,at doses from 10 to 40 nM. TCDD increased cyclooxygenase enzymes (COX)-2 expression and its downstream prostaglandin (PG) production (mainly PGE

Indexed as

AnimalsApoptosisCaspase 3Cyclooxygenase 2DinoprostoneDose-Response Relationship, DrugEndothelium, VascularEnvironmental PollutantsFemoral ArteryGene Expression RegulationHumansHuman Umbilical Vein Endothelial CellsMiceMice, Inbred C57BLMice, Knockoutp38 Mitogen-Activated Protein KinasesBcl2 protein, mouseCasp3 protein, mouseCaspase 3Cyclooxygenase 2DinoprostoneEnvironmental Pollutantsp38 Mitogen-Activated Protein KinasesPolychlorinated DibenzodioxinsProto-Oncogene Proteins c-bcl-2Ptger3 protein, mousePtgs2 protein, mouseReceptors, Prostaglandin E, EP3 SubtypeRNA, Small InterferingapoptosisBcl-2dioxinendothelial cellEP3p38 MAPK

Identifiers

PMID28699682
PMCPMC5706494
OpenAlexW2734716443

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.