Evidence map›Paper›PMID 32641583›Full record

ArticleJCI insight2020

Endothelial cell prostaglandin E2 receptor EP4 is essential for blood pressure homeostasis.

Hu Xu, Bingying Fang, Shengnan Du, Sailun Wang, Qingwei Li, Xiao Jia, Chengzhen Bao, Lan Ye, Xue Sui, Lei Qian and 7 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 35 citations in OpenAlex.

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  12. The Potential Role of Connexins in the Pathogenesis of Atherosclerosis.International journal of molecular sciences · 2023
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  14. Bioactive lipids in hypertension.Advances in pharmacology (San Diego, Calif.) · 2023
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  15. Review
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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

17 authors at 4 institutions in 2 countries.

Hu XuAdvanced Institute for Medical Sciences and.
Bingying FangAdvanced Institute for Medical Sciences and.
Shengnan DuDepartment of Pharmacology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, China.
Sailun WangAdvanced Institute for Medical Sciences and.
Qingwei LiAdvanced Institute for Medical Sciences and.
Xiao JiaAdvanced Institute for Medical Sciences and.
Chengzhen BaoAdvanced Institute for Medical Sciences and.
Lan YeAdvanced Institute for Medical Sciences and.
Xue SuiAdvanced Institute for Medical Sciences and.
Lei QianAdvanced Institute for Medical Sciences and.
Zhilin LuanAdvanced Institute for Medical Sciences and.
Guangrui YangSchool of Bioengineering, Dalian University of Technology, Dalian, China.
Feng ZhengAdvanced Institute for Medical Sciences and.
Nanping WangAdvanced Institute for Medical Sciences and.
Lihong ChenAdvanced Institute for Medical Sciences and.
Xiaoyan ZhangAdvanced Institute for Medical Sciences and.
Youfei GuanAdvanced Institute for Medical Sciences and.
Institute for Advanced Medical Research · USDalian Medical University · CNDalian University of Technology · CNZhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostaglandin E2 and its cognate EP1-4 receptors play important roles in blood pressure (BP) regulation. Herein, we show that endothelial cell-specific (EC-specific) EP4 gene-knockout mice (EC-EP4-/-) exhibited elevated, while EC-specific EP4-overexpression mice (EC-hEP4OE) displayed reduced, BP levels compared with the control mice under both basal and high-salt diet-fed conditions. The altered BP was completely abolished by treatment with l-NG-nitro-l-arginine methyl ester (l-NAME), a competitive inhibitor of endothelial nitric oxide synthase (eNOS). The mesenteric arteries of the EC-EP4-/- mice showed increased vasoconstrictive response to angiotensin II and reduced vasorelaxant response to acetylcholine, both of which were eliminated by l-NAME. Furthermore, EP4 activation significantly reduced BP levels in hypertensive rats. Mechanistically, EP4 deletion markedly decreased NO contents in blood vessels via reducing eNOS phosphorylation at Ser1177. EP4 enhanced NO production mainly through the AMPK pathway in cultured ECs. Collectively, our findings demonstrate that endothelial EP4 is essential for BP homeostasis.

Indexed as

AnimalsBlood PressureDinoprostoneEndothelial CellsEndothelium, VascularHomeostasisHypertensionMice, TransgenicNG-Nitroarginine Methyl EsterNitric Oxide Synthase Type IIIReceptors, Prostaglandin E, EP4 SubtypeDinoprostoneNG-Nitroarginine Methyl EsterNitric Oxide Synthase Type IIIReceptors, Prostaglandin E, EP4 Subtypeendothelial cellsVascular Biology

Identifiers

PMID32641583
PMCPMC7406248
OpenAlexW3040966075

What OpenQuestion holds

Textmetadata
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.