Evidence map›Paper›PMID 23723450›Full record

ArticleBlood2013

Critical role of sphingosine-1-phosphate receptor 2 (S1PR2) in acute vascular inflammation.

Guoqi Zhang, Li Yang, Gab Seok Kim, Kieran Ryan, Shulin Lu, Rebekah K O'Donnell, Katherine Spokes, Nathan Shapiro, William C Aird, Michael J Kluk and 2 more

Abstract read
In one paragraph

Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

98 citing papers in PubMed, 171 citations in OpenAlex.

  1. Trial
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  10. Regulatory T cell and endothelial cell crosstalk.Nature reviews. Immunology · 2025
    Review
  11. Targeting S1PR2 in Sepsis, One Fragmented Mitochondrion at a Time.American journal of respiratory cell and molecular biology · 2025
    Article
  12. Review
  13. Review
  14. Article
  15. Review
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  18. Article
  19. Ying and Yang of Ceramide in the Vascular Endothelium.Arteriosclerosis, thrombosis, and vascular biology · 2024
    Review
  20. Nogo-A is secreted in extracellular vesicles, occurs in blood and can influence vascular permeability.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
    Article

38 more citing papers are in PubMed but not listed here.

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

12 authors at 2 institutions in 2 countries.

Guoqi ZhangDepartments of Surgery and Emergency Medicine, Center for Vascular Biology Research, Beth Israel Deaconess Medical Center, and Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02215, USA.
Li Yang
Gab Seok Kim
Kieran Ryan
Shulin Lu
Rebekah K O'Donnell
Katherine Spokes
Nathan Shapiro
William C Aird
Michael J Kluk
Kiichiro Yano
Teresa Sanchez
Hadassah Medical Center · ILBrigham and Women's Hospital · US

Funding

Sphingolipid Signaling in Endothelial Responses to InjuryR01HL094465 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI SANCHEZ GARCIA-VAO, TERESA · 2009 to 2013
$2.1M
NHLBI NIH HHS HL094465NHLBI NIH HHS R01 HL094465
6 · The paper itself

Abstract

The endothelium, as the interface between blood and all tissues, plays a critical role in inflammation. Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid, highly abundant in plasma, that potently regulates endothelial responses through interaction with its receptors (S1PRs). Here, we studied the role of S1PR2 in the regulation of the proadhesion and proinflammatory phenotype of the endothelium. By using genetic approaches and a S1PR2-specific antagonist (JTE013), we found that S1PR2 plays a key role in the permeability and inflammatory responses of the vascular endothelium during endotoxemia. Experiments with bone marrow chimeras (S1pr2(+/+) → S1pr2(+/+), S1pr2(+/+) → S1pr2(-/-), and S1pr2(-/-) → S1pr2(+/+)) indicate the critical role of S1PR2 in the stromal compartment, in the regulation of vascular permeability and vascular inflammation. In vitro, JTE013 potently inhibited tumor necrosis factor α-induced endothelial inflammation. Finally, we provide detailed mechanisms on the downstream signaling of S1PR2 in vascular inflammation that include the activation of the stress-activated protein kinase pathway that, together with the Rho-kinase nuclear factor kappa B pathway (NF-kB), are required for S1PR2-mediated endothelial inflammatory responses. Taken together, our data indicate that S1PR2 is a key regulator of the proinflammatory phenotype of the endothelium and identify S1PR2 as a novel therapeutic target for vascular disorders.

Indexed as

Acute DiseaseAnimalsBiomarkersBlood CoagulationBlood VesselsCapillary PermeabilityEndothelium, VascularEndotoxemiaEnzyme ActivationHumansHuman Umbilical Vein Endothelial CellsImmunohistochemistryInflammationInflammation MediatorsKidneyMiceBiomarkersInflammation MediatorsJTE 013NF-kappa Bp38 Mitogen-Activated Protein KinasesPyrazolesPyridinesReceptors, Lysosphingolipid

Identifiers

PMID23723450
PMCPMC3716205
OpenAlexW2048085891

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.