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Mitochondrial Dynamics Decrease Prior to Axon Degeneration Induced by Vincristine and are Partially Rescued by
Gregory W Berbusse1, Laken C Woods2, Bhupinder P S Vohra3
1Department of Cellular Physiology and Molecular Biophysics, University of Arkansas for Medical Sciences Little Rock, AR, USA.
Frontiers in Cellular Neuroscience
|August 4, 2016
Summary
Vincristine causes axon degeneration by disrupting mitochondrial dynamics, leading to fragmentation. CytNmnat1 protects axons by maintaining normal mitochondrial structure and movement, preventing neurodegeneration.
Area of Science:
- Neuroscience
- Cell Biology
- Mitochondrial Dynamics
Background:
- Axon degeneration is a hallmark of neurodegenerative diseases like Parkinson's and Alzheimer's.
- Aberrant mitochondrial dynamics, including fission, fusion, and motility, are implicated in neurodegeneration.
- Cytosolic Nmnat1 (cytNmnat1) is known to inhibit axon degeneration but its mechanism is unclear.
Purpose of the Study:
- To investigate the role of mitochondrial dynamics and fragmentation in vincristine-induced axon degradation in dorsal root ganglia (DRG) neurons.
- To determine the effect of cytNmnat1 on mitochondrial dynamics in the context of vincristine toxicity.
Main Methods:
- Cultured dorsal root ganglia (DRG) neurons were treated with vincristine.
- Mitochondrial dynamics (fission, fusion, motility) and fragmentation were assessed.
- The impact of cytNmnat1 overexpression on these processes was evaluated.
Main Results:
- Vincristine treatment reduced mitochondrial fission, fusion, and motility, and induced fragmentation.
- These mitochondrial changes preceded observable axon degeneration.
- Overexpression of cytNmnat1 prevented axon degeneration and maintained normal mitochondrial dynamics and motility.
Conclusions:
- Alterations in mitochondrial structure and dynamics are early events in axon degeneration.
- CytNmnat1 protects against axon degeneration by preserving mitochondrial structure and dynamics against vincristine-induced damage.
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