Evidence map›Paper›PMID 18367729›Full record

ArticleAmerican journal of respiratory cell and molecular biology2008

Sphingosine 1-phosphate potentiates human lung fibroblast chemotaxis through the S1P2 receptor.

Mitsu Hashimoto, Xingqi Wang, Lijun Mao, Tetsu Kobayashi, Shin Kawasaki, Naoyoshi Mori, Myron L Toews, Hui Jung Kim, D Roselyn Cerutis, Xiangde Liu and 1 more

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Pathogenesis of Systemic Sclerosis.Frontiers in immunology · 2015
    Review
  9. The sphingosine kinase 1/sphingosine-1-phosphate pathway in pulmonary arterial hypertension.American journal of respiratory and critical care medicine · 2014
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Sphingolipid regulation of tissue fibrosis.The open rheumatology journal · 2012
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
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

11 authors at 6 institutions in 3 countries.

Mitsu HashimotoDepartment of Pathology, Nagoya University School of Medicine, Nagoya, Japan.
Xingqi Wang
Lijun Mao
Tetsu Kobayashi
Shin Kawasaki
Naoyoshi Mori
Myron L Toews
Hui Jung Kim
D Roselyn Cerutis
Xiangde Liu
Stephen I Rennard
SleepMed · USNagoya University · JPCreighton University · USSusan Thompson Buffett Foundation · USUniversity of Nebraska Medical Center · USWonkwang University Hospital · KR

Funding

CYTOKINE MODULATION OF MATRIX REMODELINGR01HL064088 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI RENNARD, STEPHEN RENNARD · 1999 to 2002
$767k
NHLBI NIH HHS HL64088-04
6 · The paper itself

Abstract

Migration of fibroblasts plays an essential role in tissue repair after injury. Sphingosine 1-phosphate (S1P) is a multifunctional mediator released by many cells that can be released in inflammation and after injury. This study evaluated the effect of S1P on fibroblast chemotaxis toward fibronectin. S1P alone did not affect fibroblast migration, but S1P enhanced fibronectin-directed chemotaxis in a concentration-dependent manner. The effect of S1P was not mimicked by dihydro (dh) S1P or the S1P(1) receptor agonist SEW2871. S1P augmentation of fibroblast chemotaxis, however, was completely blocked by JTE-013, an S1P(2) antagonist, but not by suramin, an S1P(3) antagonist. Suppression of the S1P(2) receptor by small interfering (si)RNA also completely blocked S1P augmentation of fibroblast chemotaxis to fibronectin. S1P stimulated Rho activation and focal adhesion kinase (FAK) phosphorylation, and these were also significantly inhibited by the S1P(2) receptor antagonist (JTE-013) or by S1P(2) siRNA. Further, the potentiation of S1P signaling was blocked by the Rho-kinase inhibitor Y-27632 in a concentration-dependent manner. Inhibition of FAK with siRNA reduced basal chemotaxis toward fibronectin slightly but significantly, and almost completely blocked S1P augmented chemotaxis. These results suggest that S1P-augmented fibroblast chemotaxis toward fibronectin depends on the S1P(2) receptor and requires Rho and Rho-kinase, and FAK phosphorylation. By augmenting fibroblast recruitment, S1P has the potential to modulate tissue repair after injury. The pathways by which S1P mediates this effect, therefore, represent a potential therapeutic target to affect tissue repair and remodeling.

Indexed as

ChemotaxisBase SequenceBlotting, WesternCells, CulturedDNA PrimersFibroblastsFibronectinsHumansImmunoprecipitationLungLysophospholipidsReceptors, LysosphingolipidRegenerationReverse Transcriptase Polymerase Chain ReactionRNA InterferenceSignal TransductionDNA PrimersFibronectinsLysophospholipidsReceptors, LysosphingolipidSphingosinesphingosine 1-phosphate

Identifiers

PMID18367729
PMCPMC2542450
OpenAlexW2060063932

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.