Evidence map›Paper›PMID 21504756›Full record

ArticleToxicology and applied pharmacology2011

Role of zebrafish cytochrome P450 CYP1C genes in the reduced mesencephalic vein blood flow caused by activation of AHR2.

Akira Kubota, John J Stegeman, Bruce R Woodin, Toshihiko Iwanaga, Ryo Harano, Richard E Peterson, Takeo Hiraga, Hiroki Teraoka

Abstract read
In one paragraph

Article in Toxicology and applied pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.6field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. A Review of the Functional Roles of the Zebrafish Aryl Hydrocarbon Receptors.Toxicological sciences : an official journal of the Society of Toxicology · 2020
    Review
  9. The Aryl Hydrocarbon Receptor and the Nervous System.International journal of molecular sciences · 2018
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Reproductive and developmental toxicity of dioxin in fish.Molecular and cellular endocrinology · 2012
    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

8 authors at 4 institutions in 2 countries.

Akira KubotaDepartment of Toxicology, School of Veterinary Medicine, Rakuno Gakuen University, Ebetsu 069-8501, Japan. akubota@whoi.edu
John J Stegeman
Bruce R Woodin
Toshihiko Iwanaga
Ryo Harano
Richard E Peterson
Takeo Hiraga
Hiroki Teraoka
Rakuno Gakuen University · JPWoods Hole Oceanographic Institution · USHokkaido University · JPUniversity of Wisconsin–Madison · US

Funding

Training CoreP42ES007381 · NIEHS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI HAHN, MARK E · 1995 to 2019
$46.1M
CYP Genes and the Generation of Oxidative StressR01ES015912 · NIEHS · WOODS HOLE OCEANOGRAPHIC INSTITUTION · PI STEGEMAN, JOHN J · 2007 to 2011
$3.1M
NIEHS NIH HHS 5P42ES007381NIEHS NIH HHS P42 ES007381NIEHS NIH HHS R01 ES015912NIEHS NIH HHS R01ES015912
6 · The paper itself

Abstract

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) causes various signs of toxicity in early life stages of vertebrates through activation of the aryl hydrocarbon receptor (AHR). We previously reported a sensitive and useful endpoint of TCDD developmental toxicity in zebrafish, namely a decrease in blood flow in the dorsal midbrain, but downstream genes involved in the effect are not known. The present study addressed the role of zebrafish cytochrome P450 1C (CYP1C) genes in association with a decrease in mesencephalic vein (MsV) blood flow. The CYP1C subfamily was recently discovered in fish and includes the paralogues CYP1C1 and CYP1C2, both of which are induced via AHR2 in zebrafish embryos. We used morpholino antisense oligonucleotides (MO or morpholino) to block initiation of translation of the target genes. TCDD-induced mRNA expression of CYP1Cs and a decrease in MsV blood flow were both blocked by gene knockdown of AHR2. Gene knockdown of CYP1C1 by two different morpholinos and CYP1C2 by two different morpholinos, but not by their 5 nucleotide-mismatch controls, was effective in blocking reduced MsV blood flow caused by TCDD. The same CYP1C-MOs prevented reduction of blood flow in the MsV caused by β-naphthoflavone (BNF), representing another class of AHR agonists. Whole-mount in situ hybridization revealed that mRNA expression of CYP1C1 and CYP1C2 was induced by TCDD most strongly in branchiogenic primordia and pectoral fin buds. In situ hybridization using head transverse sections showed that TCDD increased the expression of both CYP1Cs in endothelial cells of blood vessels, including the MsV. These results indicate a potential role of CYP1C1 and CYP1C2 in the local circulation failure induced by AHR2 activation in the dorsal midbrain of the zebrafish embryo.

Indexed as

Animalsbeta-NaphthoflavoneCytochrome P-450 Enzyme SystemGene Expression Regulation, DevelopmentalMesencephalonPolychlorinated DibenzodioxinsProtein BiosynthesisReceptors, Aryl HydrocarbonRegional Blood FlowZebrafishZebrafish ProteinsAHR2 protein, zebrafishbeta-NaphthoflavoneCytochrome P-450 Enzyme SystemPolychlorinated DibenzodioxinsReceptors, Aryl HydrocarbonZebrafish Proteins

Identifiers

PMID21504756
PMCPMC3143178
OpenAlexW2014373265

What OpenQuestion holds

Textmetadata
LicenceTDM
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.