Fingolimod induces the transition to a nerve regeneration promoting Schwann cell phenotype
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- 作者：André ; Heinen1 ; Felix Beyer1 ; Nevena Tzekova ; Hans-Peter Hartung ; Patrick Kü ; ry ; kuery@uni-duesseldorf.de" class="auth_mail" title="E-mail the corresponding author
- 关键词：Akt ; PKB ; protein kinase B ; BDNF ; brain derived neurotrophic factor ; cAMP ; cyclic adenosine monophosphate ; CIDP ; chronic inflammatory demyelinating polyneuropathy ; CNS ; central nervous system ; Cx32 ; connexin-32 ; DMSO ; dimethyl sulfoxide ; DRG ; dorsal root ganglia ; EAE ; experimental autoimmune encephalomyelitis ; EAN ; experimental autoimmune neuritis ; ERK ; extracellular-signal regulated kinase ; Fig ; figure ; GAP43 ; growth associated protein 43 ; GAPDH ; glyceraldehyde 3-phosphate dehydrogenase ; GBS ; G
- 刊名：Experimental Neurology
- 出版年：2015
- 出版时间：September 2015
- 年：2015
- 卷：271
- 期：Complete
- 页码：25-35
- 全文大小：1297 K
文摘
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Schwann cells act as central repair components of many nerve pathologies.
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Trans-differentiation is necessary for their conversion to repair mediating cells.
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Fingolimod promotes the generation of a repair associated Schwann cell phenotype.
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Fingolimod enhances the axon regeneration promoting potential of Schwann cells.
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Fingolimod could therefore be used for future nerve repair therapies.