Evidence map›Paper›PMID 17320059›Full record

ArticleBrain research2007

Extracellular glutamine is a critical modulator for regulatory volume increase in human glioma cells.

Nola Jean Ernest, Harald Sontheimer

Open access · greenAbstract read
In one paragraph

Article in Brain research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

15 citing papers in PubMed, 31 citations in OpenAlex.

  1. Precancer exercise capacity and metabolism during tumor development coordinate the skeletal muscle-tumor metabolic competition.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  2. Ion Channels in Glioma Malignancy.Reviews of physiology, biochemistry and pharmacology · 2021
    Review
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  8. Hydrodynamic cellular volume changes enable glioma cell invasion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    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

2 authors at 1 institution in 1 country.

Nola Jean ErnestDepartment of Neurobiology, The Civitan International Research Center, University of Alabama at Birmingham, CIRC 425, 1719 6th Avenue South, Birmingham, AL 35294, USA.
Harald Sontheimer
Civitan International · US

Funding

The Role of Ion Transport in Glioma Migration, Proliferation, and ApoptosisR01NS036692 · NINDS · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI SONTHEIMER, HARALD W · 1997 to 2024
$6.8M
PROPERTIES AND FUNCTION OF GLIA ION CHANNELSR01NS031234 · NINDS · YALE UNIVERSITY · PI SONTHEIMER, HARALD W · 1994 to 2011
$3.3M
NINDS NIH HHS R01 NS031234NINDS NIH HHS R01 NS036692
6 · The paper itself

Abstract

Mammalian cells regulate their volume to prevent unintentional changes in intracellular signaling, cell metabolism, and DNA integrity. Intentional cell volume changes occur as cells undergo proliferation, apoptosis, or cell migration. To regulate cell volume, cells use channels and transport systems to flux osmolytes across the plasma membrane followed by the obligatory movement of water. While essentially all cells are capable of regulatory volume decrease (RVD), regulatory volume increase (RVI) mechanisms have only been reported in some cell types. In this investigation, we used human glioma cells as a model system to determine conditions necessary for RVI. When exposed to hyperosmotic conditions through the addition of 30 mosM NaCl or sucrose, D54-MG and U251 glioma cell lines and glioma cells from acute patient biopsies shrunk transiently but were able to fully recover their original cell volume within 40-70 min. This ability was highly temperature sensitive and absolutely required the presence of low millimolar concentrations of l-glutamine in the extracellular solution. Other known substrates of glutamine transporters such as methyl-amino isobutyric acid (MeAIB), alanine, and threonine were unable to support RVI. The ability of cells to undergo RVI also required the presence of Na+, K+, and Cl- and was inhibited by the NKCC inhibitor, bumetanide, consistent with the involvement of a Na+/K+/2Cl- cotransporter (NKCC). Moreover, the expression of NKCC1 was demonstrated by Western blot. We concluded that regulatory volume increase in human glioma cells occurs through the uptake of Na+, K+, and Cl- by NKCC1 and is modulated by the presence of glutamine.

Indexed as

Blotting, WesternBumetanideCell Line, TumorCell SizeExtracellular SpaceGene ExpressionGlioblastomaHumansHypertonic SolutionsSodium Potassium Chloride Symporter InhibitorsSodium-Potassium-Chloride SymportersSolute Carrier Family 12, Member 2BumetanideHypertonic SolutionsSLC12A2 protein, humanSodium Potassium Chloride Symporter InhibitorsSodium-Potassium-Chloride SymportersSolute Carrier Family 12, Member 2

Identifiers

PMID17320059
PMCPMC1899165
OpenAlexW2056101675

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.