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Updated: Jun 3, 2026
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Measuring Composition of CD95 Death-Inducing Signaling Complex and Processing of Procaspase-8 in this Complex
Published on: August 2, 2021
DMSO modulates the pathway of apoptosis triggering.
Blaž Banič1, Damijan Nipič, Dušan Suput
1Institute of Pathophysiology, Faculty of Medicine, University of Ljubljana, Zaloška 4, SI-1000, Ljubljana, Slovenia.
Cellular & Molecular Biology Letters
|March 29, 2011
Summary
Dimethyl sulfoxide (DMSO) temporarily normalizes hepatocyte apoptosis susceptibility by modulating caspase-9 localization. This preapoptotic cell stress response modulation may extend primary cell culture survival.
Area of Science:
- Cell Biology
- Biochemistry
Background:
- Caspase-9 activation is crucial for initiating apoptosis.
- Cellular stress can alter protein localization, impacting cellular processes.
- Primary hepatocytes are vital for research but have limited lifespan.
Purpose of the Study:
- To investigate the role of caspase-9 distribution in apoptosis triggering.
- To determine the effect of dimethyl sulfoxide (DMSO) on caspase-9 localization and hepatocyte apoptosis.
- To explore DMSO's potential for extending primary cell culture survival.
Main Methods:
- Monitoring caspase-9 localization in primary hepatocytes under various conditions.
- Assessing caspase activity to measure apoptosis susceptibility.
- Evaluating the impact of DMSO treatment timing on caspase-9 distribution and cell survival.
Main Results:
- Caspase-9 activation is efficient only when localized in the cytosol.
- Cell stress during isolation causes caspase-9 nuclear translocation (preapoptotic stress response).
- DMSO treatment can induce temporary redistribution of caspase-9 from nuclei to cytosol, normalizing apoptosis susceptibility.
Conclusions:
- DMSO modulates the preapoptotic cell stress response by altering caspase-9 localization.
- This modulation temporarily normalizes hepatocyte susceptibility to apoptosis via the intrinsic pathway.
- DMSO's effects suggest a potential strategy for extending the lifespan of primary cell cultures.
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