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Hypoxic Preconditioning of Marrow-derived Progenitor Cells As a Source for the Generation of Mature Schwann Cells
Published on: June 14, 2017
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Axon contact-driven Schwann cell dedifferentiation.
Jennifer Soto1, Paula V Monje1
1Miami Project to Cure Paralysis and Department of Neurological Surgery, University of Miami Miller School of Medicine, Miami, Florida, 33136.
Glia
|February 25, 2017
Summary
Mature Schwann cells (SCs) dedifferentiate via a novel axon surface protein. This signal overrides differentiation cues, promoting SC dedifferentiation and proliferation, independent of common signaling pathways.
Area of Science:
- Neuroscience
- Cell Biology
- Developmental Biology
Background:
- Mature Schwann cells (SCs) possess dedifferentiation potential in adulthood.
- The mechanisms driving SC dedifferentiation remain largely unknown.
Purpose of the Study:
- To investigate the mechanisms underlying Schwann cell (SC) dedifferentiation.
- To identify potential signals from dorsal root ganglion (DRG) axons that influence SC differentiation state.
Main Methods:
- In vitro cell-based assays using cAMP-differentiated and myelinating SCs.
- Analysis of SC marker expression, proliferation, and signaling pathways (ERK, JNK).
- Characterization of the axonal dedifferentiating activity (membrane-bound, protease-sensitive).
Main Results:
- A novel membrane-bound axonal activity on DRG neurons was identified that induces SC dedifferentiation.
- This activity prevents SC differentiation and promotes proliferation, even with elevated cAMP.
- The dedifferentiating signal acts independently of neuregulin-1 and common mitogenic pathways (RTKs, ERK, JNK).
- Dedifferentiation occurred without altering Krox-20 or c-Jun expression.
Conclusions:
- Axon-derived cell surface signals can override pro-differentiating cues, driving SC dedifferentiation and proliferation.
- This novel axonal signal may regulate myelination by influencing the SC differentiated state.
