Evidence map›Paper›PMID 26374207›Full record

ArticleBrain structure & function2016

Expression of the retinoic acid catabolic enzyme CYP26B1 in the human brain to maintain signaling homeostasis.

Patrick N Stoney, Yara D Fragoso, Reem Bu Saeed, Anna Ashton, Timothy Goodman, Claire Simons, Mohamed S Gomaa, Angelo Sementilli, Leonardo Sementilli, Alexander W Ross and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Brain structure & function, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

29 citing papers in PubMed, 40 citations in OpenAlex.

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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 4 institutions in 3 countries.

Patrick N StoneyInstitute of Medical Sciences, University of Aberdeen, Aberdeen, AB25 2ZD, UK.
Yara D FragosoInstitute of Medical Sciences, University of Aberdeen, Aberdeen, AB25 2ZD, UK.
Reem Bu SaeedInstitute of Medical Sciences, University of Aberdeen, Aberdeen, AB25 2ZD, UK.
Anna AshtonInstitute of Medical Sciences, University of Aberdeen, Aberdeen, AB25 2ZD, UK.
Timothy GoodmanSchool of Biological Sciences, University of East Anglia, Norwich, NR4 7TJ, UK.
Claire SimonsMedicinal Chemistry Division, Welsh School of Pharmacy, Cardiff University, King Edward VII Avenue, Cardiff, CF10 3NB, UK.
Mohamed S GomaaMedicinal Chemistry Division, Welsh School of Pharmacy, Cardiff University, King Edward VII Avenue, Cardiff, CF10 3NB, UK.
Angelo SementilliDepartment of Physiopathology, Universidade Metropolitana de Santos, Santos, SP, Brazil.
Leonardo SementilliDepartment of Physiopathology, Universidade Metropolitana de Santos, Santos, SP, Brazil.
Alexander W RossRowett Institute of Nutrition and Health, University of Aberdeen, Greenburn Road, Bucksburn, Aberdeen, AB21 9SB, Scotland, UK.
Peter J MorganRowett Institute of Nutrition and Health, University of Aberdeen, Greenburn Road, Bucksburn, Aberdeen, AB21 9SB, Scotland, UK.
Peter J McCafferyInstitute of Medical Sciences, University of Aberdeen, Aberdeen, AB25 2ZD, UK. p.j.mccaffery@abdn.ac.uk.
University of Aberdeen · GBUniversidade Metropolitana de Santos · BRCardiff University · GBUniversity of East Anglia · GB

Funding

Wellcome TrustWellcome Trust WT081633MA-NCE
6 · The paper itself

Abstract

Retinoic acid (RA) is a potent regulator of gene transcription via its activation of a set of nuclear receptors controlling transcriptional activation. Precise maintenance of where and when RA is generated is essential and achieved by local expression of synthetic and catabolic enzymes. The catabolic enzymes Cyp26a1 and Cyp26b1 have been studied in detail in the embryo, where they limit gradients of RA that form patterns of gene expression, crucial for morphogenesis. This paracrine role of RA has been assumed to occur in most tissues and that the RA synthetic enzymes release RA at a site distant from the catabolic enzymes. In contrast to the embryonic CNS, relatively little is known about RA metabolism in the adult brain. This study investigated the distribution of Cyp26a1 and Cyp26b1 transcripts in the rat brain, identifying several novel regions of expression, including the cerebral cortex for both enzymes and striatum for Cyp26b1. In vivo use of a new and potent inhibitor of the Cyp26 enzymes, ser 2-7, demonstrated a function for endogenous Cyp26 in the brain and that hippocampal RA levels can be raised by ser 2-7, altering the effect of RA on differential patterning of cell proliferation in the hippocampal region of neurogenesis, the subgranular zone. The expression of CYP26A1 and CYP26B1 was also investigated in the adult human brain and colocalization of CYP26A1 and the RA synthetic enzyme RALDH2 indicated a different, autocrine role for RA in human hippocampal neurons. Studies with the SH-SY5Y human neuroblastoma cell line implied that the co-expression of RA synthetic and catabolic enzymes maintains retinoid homeostasis within neurons. This presents a novel view of RA in human neurons as part of an autocrine, intracellular signaling system.

Indexed as

Autocrine CommunicationHomeostasisParacrine CommunicationAldehyde Dehydrogenase 1 FamilyAnimalsBrainCell Line, TumorCell ProliferationCerebral CortexCorpus StriatumFemaleGene ExpressionHippocampusHumansMaleMiddle AgedAldehyde Dehydrogenase 1 FamilyALDH1A2 protein, humanCYP26A1 protein, humanCYP26B1 protein, humanRetinal DehydrogenaseRetinoic Acid 4-HydroxylaseTretinoinCYP26A1CYP26B1Dentate gyrusGradientHippocampusInfrapyramidalRetinoic acid catabolismSuprapyramidal

Identifiers

PMID26374207
PMCPMC4920859
OpenAlexW2170161650

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.