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

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

Research Abstract Table of Contents

Jump to the:

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

Nola Jean Ernest,Christa W Habela,Harald Sontheimer,

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.

Cytoplasmic condensation is both necessary and sufficient to induce apoptotic cell death. Publishing Authors By Initials

NJ Ernest,CW Habela,H Sontheimer,

For similar abstracts research abstracts see: abstracts research

PUBMED ID PMID:

MEDLINE DATE:

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

PUBLICATION TYPE: Journal Article

Journal: Journal of cell science

VOLUME: 121

Page Numbers: 290-7

Journal Abbreviation: J. Cell. Sci.

ISSN: 0021-9533

DAY: 15

MONTH: 01

YEAR: 2008

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

Number of References:

LANGUAGE: eng

NlmUniqueID: 52457

Cytoplasmic condensation is both necessary and sufficient to induce apoptotic cell death. Keywords Mesh Terms:

KEYWORDS:

MESH TERMS:

Chemical & Substance for Abstract: Cytoplasmic condensation is both necessary and sufficient to induce apoptotic cell death. Information

Substance Name:

Registry Number:

Grant and Affiliation Information for Cytoplasmic condensation is both necessary and sufficient to induce apoptotic cell death.

AFFILIATION: Department of Neurobiology, the Civitan International Research Center, and the Center for Glial Biology in Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA.

Country: England

AGENCY:

GRANT:

ACRONYM:

MEDLINETA: J Cell Sci

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

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

• A glossary of modern health care economics: platitudes and principles gleaned from the first year's education of a new academic health care delivery center department head.
• A role for glutamate in growth and invasion of primary brain tumors.
• A role for ubiquitin in the spliceosome assembly pathway.
• A systematic review of juvenile-onset clinically amyopathic dermatomyositis.
• An inside job for siRNAs.
• An unexpected role for ion channels in brain tumor metastasis.
• Another view concerning the proposal to change the name of the American Academy of Dermatology.
• Antibodies inside our keratinocytes?
• Autocrine glutamate signaling promotes glioma cell invasion.
• BK channels are linked to inositol 1,4,5-triphosphate receptors via lipid rafts: a novel mechanism for coupling [Ca(2+)](i) to ion channel activation.
• Chronic penile ulceration in a 72-year-old man.
• ClC3 Is a Critical Regulator of the Cell Cycle in Normal and Malignant Glial Cells.
• Cutaneous lupus erythematosus: molecular and cellular basis of clinical findings.
• Cytoplasmic condensation is both necessary and sufficient to induce apoptotic cell death.
• Differential distribution of Kir4.1 in spinal cord astrocytes suggests regional differences in K+ homeostasis.
• Expression and function of water channels (aquaporins) in migrating malignant astrocytes.
• Extracellular glutamine is a critical modulator for regulatory volume increase in human glioma cells.
• Immunobiological significance of the Ro/SSA antigen-antibody system.
• Inhibition of transient receptor potential canonical channels impairs cytokinesis in human malignant gliomas.
• Questions answered and a $1 million question raised concerning lupus erythematosus tumidus: is routine laboratory surveillance testing during treatment with hydroxychloroquine for skin disease really necessary.
• Relative contribution of chloride channels and transporters to regulatory volume decrease in human glioma cells.
• Review: Statins reduce all-cause mortality in elderly patients with coronary heart disease.
• Role for calcium-activated potassium channels (BK) in growth control of human malignant glioma cells.
• Role of Kir4.1 channels in growth control of glia.
• Sarcoidal alopecia as a mimic of discoid lupus erythematosus.
• Suicide by advance directive?
• The anticardiolipin syndrome. A new way to slice an old pie, or a new pie to slice?