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Experimental Demyelination and Remyelination of Murine Spinal Cord by Focal Injection of Lysolecithin
Published on: March 26, 2015
The Role of Peripheral Myelin Protein 2 in Remyelination
Mark Stettner1, Jennifer Zenker2, Fabian Klingler3
1Department of Neurology, University Hospital Essen, Essen, Germany. mark.stettner@uk-essen.de.
Abstract:
The protein component of the myelin layer is essential for all aspects of peripheral nerves, and its deficiency can lead to structural and functional impairment. The presence of peripheral myelin protein 2 (P2, PMP2, FABP8, M-FABP) in Schwann cells has been known for decades and shown recently to be involved in the lipid homeostasis in the peripheral neural system. However, its precise role during de- and remyelination has yet to be elucidated. To this end, we assessed remyelination after sciatic nerve crush injury in vivo, and in an experimental de/remyelination ex vivo myelinating culture model in P2-deficient (P2 -/- ) and wild-type (WT) animals. In vivo, the nerve crush paradigm revealed temporal structural and functional changes in P2 -/- mice as compared to WT animals. Concomitantly, P2 -/- DRG cultures demonstrated the presence of shorter internodes and enlarged nodes after ex vivo de/remyelination. Together, these data indicate that P2 may play a role in remyelination of the injured peripheral nervous system, presumably by affecting the nodal and internodal configuration.
Insights
Peripheral myelin protein 2 (P2) is crucial for peripheral nerve repair. P2 deficiency impairs remyelination and alters nerve structure after injury, highlighting its role in nerve regeneration.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Myelin sheath proteins are vital for peripheral nerve function.
- Peripheral myelin protein 2 (PMP2) is present in Schwann cells and involved in lipid homeostasis.
- The specific role of P2 in nerve de- and remyelination remains unclear.
Purpose of the Study:
- To investigate the role of P2 in peripheral nerve remyelination following injury.
- To compare remyelination processes in P2-deficient and wild-type animals.
Main Methods:
- Sciatic nerve crush injury model in vivo.
- Ex vivo myelinating culture model using dorsal root ganglion (DRG) from P2-deficient (P2-/-) and wild-type (WT) mice.
- Assessment of structural and functional changes during remyelination.
Main Results:
- P2-/- mice exhibited temporal structural and functional deficits compared to WT after nerve crush.
- Ex vivo de/remyelination cultures from P2-/- mice showed shorter internodes and enlarged nodes.
- These findings suggest P2 influences nodal and internodal structure during repair.
Conclusions:
- P2 plays a significant role in the remyelination of injured peripheral nerves.
- P2 appears to regulate the nodal and internodal configuration during nerve repair.
- These findings contribute to understanding peripheral nerve regeneration mechanisms.

