Evidence map›Paper›PMID 17250626›Full record

ArticleAlcoholism, clinical and experimental research2007

Ethanol regulates angiogenic cytokines during neural development: evidence from an in vitro model of mitogen-withdrawal-induced cerebral cortical neuroepithelial differentiation.

Cynthia Camarillo, Leena S Kumar, Shameena Bake, Farida Sohrabji, Rajesh C Miranda

Open access · bronzeAbstract read
In one paragraph

Article in Alcoholism, clinical and experimental research, 2007. 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
5.0field-weighted citation impact, top 6% 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, 42 citations in OpenAlex.

  1. Article
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  5. Review
  6. Article
  7. Toxicant and teratogenic effects of prenatal alcohol.Current opinion in toxicology · 2019
    Article
  8. Article
  9. Article
  10. Neuroimmune mechanisms of alcohol and drug addiction.International review of neurobiology · 2014
    Review
  11. Article
  12. Article
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  15. Article
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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

5 authors at 2 institutions in 1 country.

Cynthia CamarilloTexas A&M Health Science Center, College of Medicine, Department Neuroscience and Experimental Therapeutics, College Station, USA.
Leena S Kumar
Shameena Bake
Farida Sohrabji
Rajesh C Miranda
Texas A&M Health Science Center · USTexas A&M University · US

Funding

Fetal Alcohol Exposure and NeurodevelopmentR01AA013440 · NIAAA · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI MIRANDA, RAJESH C · 2002 to 2012
$2.7M
Fetal Alcohol Exposure and NeurodevelopmentR56AA013440 · NIAAA · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI MIRANDA, RAJESH C · 2007 to 2007
$292k
NIAAA NIH HHS AA13440NIAAA NIH HHS R01 AA013440NIAAA NIH HHS R56 AA013440
6 · The paper itself

Abstract

backgroundHeavy alcohol consumption during pregnancy can cause significant mental retardation and brain damage. We recently showed that ethanol depletes reserve cerebral cortical stem cell capacity. Moreover, proliferating neuroepithelial cells exposed to ethanol were resistant to subsequent retinoic acid-induced differentiation. Emerging evidence suggests that cytokines play a crucial growth-promoting role in the developing neural tube.

methodsWe cultured murine cortical neurosphere cultures in control or ethanol-supplemented mitogenic medium, to mimic alcohol exposure during the period of neuroepithelial proliferation. Cultures were then treated with a step-wise mitogen-withdrawal, integrin-activation model to mimic subsequent phases of neuronal migration and early differentiation. We examined the impact of alcohol exposure during neurogenesis on the secretion of inflammatory and growth-promoting cytokines.

resultsCortical neurosphere cultures exhibit increasingly complex differentiation phenotypes in response to step-wise mitogen-withdrawal and laminin exposure. Some inflammation-modulating cytokines were secreted independent of differentiation state. However, chemotactic cytokines were specifically secreted at high levels, as a function of differentiation stage. monocyte chemotactic protein-1, vascular endothelial growth factor-A, and interleukin (IL)-10 were coordinately decreased during differentiation compared with neuroepithelial proliferation, while granulocyte macrophage-colony stimulating factor (GM-CSF) was induced during differentiation, compared with the neuroepithelial proliferation period. Ethanol exposure during the period of neuroepithelial proliferation prevented the early differentiation-induced increase in GM-CSF while inducing differentiation-associated increase in IL-12 secretion.

conclusionEmbryonic cerebral cortical neuroepithelial-derived precursors secrete high levels of several angiogenic and neural-growth-promoting cytokines as they differentiate into neurons. Our data collectively suggest that ethanol exposure during the period of neuroepithelial proliferation significantly disrupts cytokine signals that are required for the support of emerging neurovascular networks, and the maintenance of neural stem cell beds.

Indexed as

Angiogenic ProteinsAnimalsCell DifferentiationCell ProliferationCells, CulturedCentral Nervous System DepressantsCerebral CortexChemokine CCL2CytokinesEthanolFemaleGranulocyte-Macrophage Colony-Stimulating FactorInterleukin-10Interleukin-12MiceMice, Inbred C57BLAngiogenic ProteinsCentral Nervous System DepressantsChemokine CCL2CytokinesEthanolGranulocyte-Macrophage Colony-Stimulating FactorInterleukin-10Interleukin-12Vascular Endothelial Growth Factor A

Identifiers

PMID17250626
PMCPMC2909106
OpenAlexW2147822524

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Registered trials

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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.