Evidence map›Paper›PMID 24509627›Full record

ArticleScientific reports2014

Predominant role of cytosolic phospholipase A2α in dioxin-induced neonatal hydronephrosis in mice.

Wataru Yoshioka, Tatsuya Kawaguchi, Nozomi Fujisawa, Keiko Aida-Yasuoka, Takao Shimizu, Fumio Matsumura, Chiharu Tohyama

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.5field-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

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Mechanisms of Developmental Toxicity of Dioxins and Related Compounds.International journal of molecular sciences · 2019
    Review
  3. Article
  4. Article
  5. Roles of cytosolic phospholipase AArchives of toxicology · 2018
    Article
  6. Review
  7. 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

7 authors at 2 institutions in 2 countries.

Wataru Yoshioka1] Laboratory of Environmental Health Sciences, Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan [2] Department of Pathophysiology, Tokyo University of Pharmacy and Life Sciences, Tokyo 192-0392, Japan.
Tatsuya KawaguchiLaboratory of Environmental Health Sciences, Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan.
Nozomi FujisawaLaboratory of Environmental Health Sciences, Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan.
Keiko Aida-YasuokaLaboratory of Environmental Health Sciences, Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan.
Takao ShimizuDepartment of Biochemistry and Molecular Biology, Faculty of Medicine, The University of Tokyo, Tokyo 113-0033, Japan.
Fumio MatsumuraDepartment of Environmental Toxicology and Center for Environmental Health Sciences, University of California, Davis, CA 95616, USA.
Chiharu TohyamaLaboratory of Environmental Health Sciences, Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan.
The University of Tokyo · JPUniversity of California, Davis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hydronephrosis is a common disease characterized by dilation of the renal pelvis and calices, resulting in loss of kidney function in the most severe cases. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) induces nonobstructive hydronephrosis in mouse neonates through upregulation of prostaglandin E2 (PGE2) synthesis pathway consisting of cyclooxygenase-2 (COX-2) and microsomal prostaglandin E synthase-1 (mPGES-1) by a yet unknown mechanism. We here studied possible involvement of cytosolic phospholipase A2α (cPLA2α) in this mechanism. To this end, we used a cPLA2α-null mouse model and found that cPLA2α has a significant role in the upregulation of the PGE2 synthesis pathway through a noncanonical pathway of aryl hydrocarbon receptor. This study is the first to demonstrate the predominant role of cPLA2α in hydronephrosis. Elucidation of the pathway leading to the onset of hydronephrosis using the TCDD-exposed mouse model will deepen our understanding of the molecular basis of nonobstructive hydronephrosis in humans.

Indexed as

AnimalsCyclooxygenase 2Cytochrome P-450 CYP1A1DinoprostoneDisease Models, AnimalFemaleGene ExpressionGroup IV Phospholipases A2HydronephrosisInsulin-Like Growth Factor Binding Protein 1Intramolecular OxidoreductasesKidneyMaleMiceMice, Inbred C57BLMice, KnockoutCyclooxygenase 2Cytochrome P-450 CYP1A1DinoprostoneGroup IV Phospholipases A2Insulin-Like Growth Factor Binding Protein 1Intramolecular OxidoreductasesPolychlorinated DibenzodioxinsProstaglandin-E SynthasesPTGES protein, humanPtges protein, mousePtgs2 protein, mouseReceptors, Aryl HydrocarbonRNA, Messenger

Identifiers

PMID24509627
PMCPMC3918923
OpenAlexW2005861385

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.