| Literature DB >> 28447247 |
Mark Stettner1, Jennifer Zenker2, Fabian Klingler3, Fabian Szepanowski4, Hans-P Hartung3, Anne K Mausberg4, Christoph Kleinschnitz4, Roman Chrast5, Bernd C Kieseier3.
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.Entities:
Keywords: CIDP; Chronic inflammatory demyelinating neuropathy; Dorsal root ganglia; Nerve crush injury; Neuropathy; P2; Peripheral myelin
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Year: 2017 PMID: 28447247 DOI: 10.1007/s10571-017-0494-0
Source DB: PubMed Journal: Cell Mol Neurobiol ISSN: 0272-4340 Impact factor: 5.046