Evidence map›Paper›PMID 24463961›Full record

ArticleClinical and experimental nephrology2014

Sphingosine-1-phosphate induces differentiation of cultured renal tubular epithelial cells under Rho kinase activation via the S1P2 receptor.

Sho Ishizawa, Junko Takahashi-Fujigasaki, Yasushi Kanazawa, Keiichiro Matoba, Daiji Kawanami, Tamotsu Yokota, Takeo Iwamoto, Naoko Tajima, Yoshinobu Manome, Kazunori Utsunomiya

Erratum issuedAbstract read
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In one paragraph

Article in Clinical and experimental nephrology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

24 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Sphingolipid signaling in kidney diseases.American journal of physiology. Renal physiology · 2025
    Review
  5. Review
  6. Review
  7. Article
  8. Implications of Sphingolipid Metabolites in Kidney Diseases.International journal of molecular sciences · 2022
    Review
  9. Review
  10. Review
  11. Loss ofHypertension (Dallas, Tex. : 1979) · 2020
    Article
  12. Article
  13. Lysophosphatidic Acid Signaling in Diabetic Nephropathy.International journal of molecular sciences · 2019
    Review
  14. Review
  15. Article
  16. Frontiers in genetics · 2019
    Article
  17. Sphingosine-1-phosphate pathway in renal fibrosis.American journal of physiology. Renal physiology · 2018
    Review
  18. Article
  19. Article
  20. Translational Aspects of Sphingolipid Metabolism in Renal Disorders.International journal of molecular sciences · 2017
    Review
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Sho IshizawaDivision of Diabetes, Metabolism and Endocrinology, Department of Internal Medicine, The Jikei University School of Medicine, 3-25-8 Nishishinbashi, Minato-ku, Tokyo, 105-8461, Japan, ishizawa@jikei.ac.jp.
Junko Takahashi-Fujigasaki
Yasushi Kanazawa
Keiichiro Matoba
Daiji Kawanami
Tamotsu Yokota
Takeo Iwamoto
Naoko Tajima
Yoshinobu Manome
Kazunori Utsunomiya
Jikei University School of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSphingosine-1-phosphate (S1P) is reportedly involved in the pathogenesis of kidney disease; however, the precise role played by S1P in renal disorders still remains controversial. Rho kinase plays an important role in the development of diabetic nephropathy by inducing glomerular and tubulointerstitial fibrosis. Rho kinase is known to be stimulated by S1P through its specific receptor, S1P2 receptor (S1P2). Hence, we investigated whether S1P-S1P2 signaling plays a role in the epithelial-mesenchymal transition (EMT) through Rho kinase activation in renal tubules.

methodTo characterize the distribution of the S1P2, an immunohistochemical examination of the receptor was performed in the kidney of the non-diabetic and diabetic mice. Next, we examined Rho kinase activity as well as E-cadherin and alpha-smooth muscle actin (α-SMA) expression by real-time RT-PCR and western blotting in cultured rat tubular epithelial cells under S1P stimulation with and without a Rho kinase inhibitor and an S1P2 blocker. In addition, the distribution of E-cadherin and α-SMA was examined by immunocytochemistry.

resultS1P2 was expressed mainly in the renal tubules; expression was intense in collecting ducts and distal tubules compared to other segments. S1P induced activation of Rho kinase through the S1P2, which changed the distribution of E-cadherin and increased the expression of α-SMA.

conclusionRho kinase activation by S1P via S1P2 initiated EMT changes in cultured renal tubular cells. Our results suggest that excessive stimulation of S1P might facilitate renal fibrosis via activation of Rho kinase through S1P2.

Indexed as

ActinsAnimalsCadherinsCell DifferentiationCells, CulturedEpithelial CellsEpithelial-Mesenchymal TransitionKidney TubulesLysophospholipidsMaleMiceMice, KnockoutReceptors, LeptinReceptors, Lysosphingolipidrho-Associated KinasesSphingosineActinsalpha-smooth muscle actin, mouseCadherinsLysophospholipidsReceptors, LeptinReceptors, Lysosphingolipidrho-Associated KinasesSphingosinesphingosine 1-phosphate

Identifiers

PMID24463961
OpenAlexW2105730373

What OpenQuestion holds

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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.