Evidence map›Paper›PMID 27146468›Full record

ArticleBMC genomics2016

Temporal Dysynchrony in brain connectivity gene expression following hypoxia.

Brett Milash, Jingxia Gao, Tamara J Stevenson, Jong-Hyun Son, Tiffanie Dahl, Joshua L Bonkowsky

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. 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

6 authors at 2 institutions in 1 country.

Brett MilashBioinformatics Shared Resource, Huntsman Cancer Institute, Salt Lake City, USA.
Jingxia GaoDepartment of Pediatrics, University of Utah, 295 Chipeta Way, 84108, Salt Lake City, UT, USA.
Tamara J StevensonDepartment of Pediatrics, University of Utah, 295 Chipeta Way, 84108, Salt Lake City, UT, USA.
Jong-Hyun SonDepartment of Pediatrics, University of Utah, 295 Chipeta Way, 84108, Salt Lake City, UT, USA.
Tiffanie DahlDepartment of Pediatrics, University of Utah, 295 Chipeta Way, 84108, Salt Lake City, UT, USA.
Joshua L BonkowskyDepartment of Pediatrics, University of Utah, 295 Chipeta Way, 84108, Salt Lake City, UT, USA. joshua.bonkowsky@hsc.utah.edu.
University of Utah · USHuntsman Cancer Institute · US

Funding

UTAH REGIONAL CANCER CENTERP30CA042014 · NCI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Jared P Rutter · 1986 to 2026
$72.6M
Trans-Cellular Activation of Transcription to Analyze Dopaminergic Axon ReorganizDP2MH100008 · NIMH · UNIVERSITY OF UTAH · PI BONKOWSKY, JOSH LEITCH · 2012 to 2012
$2.2M
Mechanisms of Serotonergic Regulation for Connectivity DevelopmentR21MH107039 · NIMH · UNIVERSITY OF UTAH · PI BONKOWSKY, JOSH LEITCH · 2015 to 2016
$410k
NCI NIH HHS P30 CA042014NIMH NIH HHS DP2 MH100008NIMH NIH HHS R21 MH107039
6 · The paper itself

Abstract

backgroundDespite the fundamental biological importance and clinical relevance of characterizing the effects of chronic hypoxia exposure on central nervous system (CNS) development, the changes in gene expression from hypoxia are unknown. It is not known if there are unifying principles, properties, or logic in the response of the developing CNS to hypoxic exposure. Here, we use the small vertebrate zebrafish (Danio rerio) to study the effects of hypoxia on connectivity gene expression across development. We perform transcriptional profiling at high temporal resolution to systematically determine and then experimentally validate the response of CNS connectivity genes to hypoxia exposure.

resultsWe characterized mRNA changes during development, comparing the effects of chronic hypoxia exposure at different time-points. We focused on changes in expression levels of a subset of 1270 genes selected for their roles in development of CNS connectivity, including axon pathfinding and synapse formation. We found that the majority of CNS connectivity genes were unaffected by hypoxia. However, for a small subset of genes hypoxia significantly affected their gene expression profiles. In particular, hypoxia appeared to affect both the timing and levels of expression, including altering expression of interacting gene pairs in a fashion that would potentially disrupt normal function.

conclusionsOverall, our study identifies the response of CNS connectivity genes to hypoxia exposure during development. While for most genes hypoxia did not significantly affect expression, for a subset of genes hypoxia changed both levels and timing of expression. Importantly, we identified that some genes with interacting proteins, for example receptor/ligand pairs, had dissimilar responses to hypoxia that would be expected to interfere with their function. The observed dysynchrony of gene expression could impair the development of normal CNS connectivity maps.

Indexed as

Gene Regulatory NetworksAnimalsConnectomeGene Expression ProfilingGene Expression Regulation, DevelopmentalHypoxia, BrainSequence Analysis, RNAZebrafishZebrafish ProteinsZebrafish ProteinsAxon pathfindingConnectivityHypoxiaSynapseZebrafish

Identifiers

PMID27146468
PMCPMC4857255
OpenAlexW2345451766

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.