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Published on: October 11, 2012
Differential regulation of the mitochondrial and death receptor pathways in neural stem cells
Christoffer Tamm1, John D Robertson, Eric Sleeper
1Institute of Environmental Medicine, Division of Toxicology and Neurotoxicology, Karolinska Institutet, 71 77 Stockholm, Sweden.
Abstract:
Despite an increasing interest in neural stem cell (NSC) research, relatively little is known about the biochemical regulation of cell death pathways in these cells. We demonstrate here, using murine-derived multipotent C17.2 NSCs, that cells undergo mitochondria-mediated cell death in response to apoptotic stimuli such as oxidative stress induced by 2,3-dimethoxy-1,4-naphthoquinone (DMNQ). In particular, treated cells exhibited apoptotic features, including Bax translocation, cytochrome c release, activation of caspase-9 and -3, chromatin condensation and DNA fragmentation. Although C17.2 cells possess the Fas receptor and express procaspase-8, agonistic Fas mAb treatment failed to induce apoptosis. Fas treatment activated the extracellular signal-regulated protein kinase (ERK) pathway, which may have an antiapoptotic as well as a growth stimulating role. Combined, our findings indicate that while NSCs are sensitive to cytotoxic stimuli that involve an engagement of mitochondria, Fas treatment does not induce death and may have an alternative role.
Insights
Neural stem cells (NSCs) undergo mitochondria-mediated cell death from oxidative stress. However, Fas receptor stimulation does not induce apoptosis in these cells, suggesting alternative roles for Fas signaling in NSCs.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Neural stem cell (NSC) research is growing, but biochemical regulation of cell death pathways remains poorly understood.
- Understanding cell death mechanisms in NSCs is crucial for regenerative medicine and neuroscience.
Purpose of the Study:
- To investigate the mechanisms of cell death in multipotent neural stem cells (NSCs).
- To determine the role of mitochondria and Fas receptor signaling in NSC apoptosis.
Main Methods:
- Murine-derived multipotent C17.2 NSCs were used.
- Cells were treated with apoptotic stimuli like 2,3-dimethoxy-1,4-naphthoquinone (DMNQ) and Fas agonistic mAb.
- Apoptotic features, including Bax translocation, cytochrome c release, caspase activation, and DNA fragmentation, were analyzed.
- Extracellular signal-regulated kinase (ERK) pathway activation was assessed.
Main Results:
- DMNQ-induced oxidative stress triggered mitochondria-mediated cell death in C17.2 NSCs.
- Key apoptotic markers such as Bax translocation, cytochrome c release, and caspase activation were observed.
- Fas receptor stimulation did not induce apoptosis, despite the presence of Fas receptor and procaspase-8.
- Fas treatment led to the activation of the extracellular signal-regulated protein kinase (ERK) pathway.
Conclusions:
- Neural stem cells are susceptible to cytotoxic stimuli engaging mitochondria.
- Fas receptor signaling does not trigger apoptosis in these NSC models.
- ERK pathway activation by Fas may play an antiapoptotic or growth-promoting role in neural stem cells.
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