Evidence map›Paper›PMID 18198188›Full record

ArticleJournal of cell science2008

Cytoplasmic condensation is both necessary and sufficient to induce apoptotic cell death.

Nola Jean Ernest, Christa W Habela, Harald Sontheimer

Abstract read
In one paragraph

Article in Journal of cell science, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
–field-weighted citation impact
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

39 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. In vitro cell cycle oscillations exhibit a robust and hysteretic response to changes in cytoplasmic density.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Ion Channels in Glioma Malignancy.Reviews of physiology, biochemistry and pharmacology · 2021
    Review
  12. Article
  13. Review
  14. Article
  15. Relevance and Regulation of Cell Density.Trends in cell biology · 2020
    Review
  16. Review
  17. A Reverse-Osmosis Model of Apoptotic Shrinkage.Frontiers in cell and developmental biology · 2020
    Article
  18. Article
  19. Cell Cycle Regulation by CaInternational journal of molecular sciences · 2018
    Article
  20. 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

3 authors.

Nola Jean ErnestDepartment of Neurobiology, Civitan International Research Center, Center for Glial Biology in Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Christa W Habela
Harald Sontheimer

Funding

Viral and molecular chemotherapy of malignant CNS tumorsP50CA097247 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GILLESPIE, G. YANCEY · 2002 to 2009
$13.5M
Alabama Neuroscience Blueprint Core CenterP30NS057098 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SWEATT, JOHN DAVID · 2006 to 2010
$9.5M
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
NCI NIH HHS P50 CA097247NCI NIH HHS P50CA97247NINDS NIH HHS P30 NS057098NINDS NIH HHS R01 NS031234NINDS NIH HHS R01 NS036692NINDS NIH HHS R01NS31234NINDS NIH HHS R01NS36692
6 · The paper itself

Abstract

Programmed cell death (apoptosis) is important in tissue maintenance. Hallmarks of apoptosis include caspase activation, DNA fragmentation and an overall reduction in cell volume. Whether this apoptotic volume decrease (AVD) is a mere response to initiators of apoptosis or whether it is functionally significant is not clear. In this study, we sought to answer this question using human malignant glioma cells as a model system. In vivo, high grade gliomas demonstrate an increased percentage of apoptotic cells as well as upregulation of death ligand receptors. By dynamically monitoring cell volume, we show that the induction of apoptosis, via activation of either the intrinsic or extrinsic pathways with staurosporine or TRAIL, respectively, resulted in a rapid AVD in D54-MG human glioma cells. This decrease in cell volume could be prevented by inhibiting the efflux of Cl(-) through channels. Such suppression of AVD also reduced the activation of caspases 3, 8 and 9 and suppressed DNA fragmentation. Importantly, experimental manipulations that reduce the cell volume to 70% of the original volume for periods of at least 3 hours were sufficient to initiate apoptosis even in the absence of death ligands. Hence, this data suggests that cell condensation is both necessary and sufficient for the induction of apoptosis.

Indexed as

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic AcidApoptosisCaspasesCell DeathCell Line, TumorCell SizeChloridesCytoplasmDNA FragmentationGliomaHumansIon TransportModels, BiologicalRecombinant ProteinsStaurosporineTNF-Related Apoptosis-Inducing Ligand4,4'-Diisothiocyanostilbene-2,2'-Disulfonic AcidCaspasesChloridesRecombinant ProteinsStaurosporineTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, human

Identifiers

PMID18198188
PMCPMC2561226

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.