Evidence map›Paper›PMID 30413562›Full record

ArticleMolecular & cellular proteomics : MCP2019

Proteomic Analysis of Baboon Cerebral Artery Reveals Potential Pathways of Damage by Prenatal Alcohol Exposure.

Shivantika Bisen, David Kakhniashvili, Daniel L Johnson, Anna N Bukiya

Open access · hybridAbstract read
In one paragraph

Article in Molecular & cellular proteomics : MCP, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Prenatal Alcohol Exposure and Mitochondrial Function in the Brain.Advances in experimental medicine and biology · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Fetal Cerebral Artery Mitochondrion as Target of Prenatal Alcohol Exposure.International journal of environmental research and public health · 2019
    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

4 authors at 1 institution in 1 country.

Shivantika BisenDepartment of Pharmacology, College of Medicine, University of Tennessee Health Science Center, 71 S. Manassas St., #205, Memphis, TN, 38103.
David KakhniashviliProteomics Core, University of Tennessee Health Science Center, 71 S. Manassas St., #110, Memphis, TN, 38103.
Daniel L JohnsonMolecular Bioinformatics Core, University of Tennessee Health Science Center, 71 S. Manassas St., #110, Memphis, TN, 38103.
Anna N BukiyaDepartment of Pharmacology, College of Medicine, University of Tennessee Health Science Center, 71 S. Manassas St., #205, Memphis, TN, 38103;. Electronic address: abukiya@uthsc.edu.
University of Tennessee Health Science Center · US

Funding

Baboon Research Resource ProgramP40OD010988 · OD · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI BANKS, RON E · 2012 to 2018
$9.0M
Fetal cerebrovascular eCB system as a target of maternal alcohol consumptionR21AA022433 · NIAAA · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI BUKIYA, ANNA · 2014 to 2015
$387k
NIAAA NIH HHS R21 AA022433NIH HHS P40 OD010988
6 · The paper itself

Abstract

Alcohol is one of the most widely misused substances in the world. Alcohol consumption by pregnant women often results in an array of fetal developmental abnormalities, but the damage to the fetus by alcohol remains poorly understood. The limited knowledge regarding the molecular targets of alcohol in the developing fetus constitutes one of the major obstacles in developing effective pharmacological interventions that could prevent fetal damage after alcohol consumption by pregnant women. The fetal cerebral artery is emerging as an important mediator of fetal cerebral damage by maternal alcohol drinking. In the present work, we conduct proteomics analysis of cerebral (basilar) artery lysates of near-term fetal baboons to search for protein targets of fetal alcohol exposure. Our study demonstrates that 3 episodes of binge alcohol exposure during the second trimester-equivalent of human pregnancy are sufficient to render profound changes in fetal cerebral artery proteome. These changes persisted, as they were detected in near-term fetuses. In particular, the relative abundance of 238 proteins differed significantly between control and alcohol-exposed fetuses. Enrichment analysis pointed at the group of metabolic activity proteins as a major class targeted by alcohol. Western blotting confirmed upregulation of the aldehyde dehydrogenase 6 family member A1 (ALDH6A1) in cerebral artery lysates from alcohol-exposed fetuses. This upregulation translated to greater ALDH activity of cerebral artery lysate of near-term fetuses following prenatal alcohol exposure when compared with controls.

Indexed as

AnimalsCerebral ArteriesDisease Models, AnimalFemaleHumansMetabolic Networks and PathwaysPapioPregnancyPrenatal Exposure Delayed EffectsProtein Interaction MapsProteomicsAlcohol in UteroAnimal ModelsBinge DrinkingCardiovascular Function or BiologyFetal Alcohol Syndrome and Spectrum DisordersMass SpectrometryMaternal DrinkingMitochondria Function or BiologyNetworksPharmacologyPhysiologyPregnancyPrenatal Alcohol Exposure

Identifiers

PMID30413562
PMCPMC6356072
OpenAlexW2899773833

What OpenQuestion holds

Textmetadata
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.