Delaying histone deacetylase response to injury accelerates conversion into repair Schwann cells and nerve regeneration

Valérie Brügger, Mert Duman, Maëlle Bochud, Emmanuelle Münger, Manfred Heller, Sophie Ruff and Claire Jacob ()
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Valérie Brügger: University of Fribourg
Mert Duman: University of Fribourg
Maëlle Bochud: University of Fribourg
Emmanuelle Münger: University of Fribourg
Manfred Heller: Proteomics and Mass Spectrometry Core Facility, University of Bern
Sophie Ruff: University of Fribourg
Claire Jacob: University of Fribourg

Nature Communications, 2017, vol. 8, issue 1, 1-16

Abstract: Abstract The peripheral nervous system (PNS) regenerates after injury. However, regeneration is often compromised in the case of large lesions, and the speed of axon reconnection to their target is critical for successful functional recovery. After injury, mature Schwann cells (SCs) convert into repair cells that foster axonal regrowth, and redifferentiate to rebuild myelin. These processes require the regulation of several transcription factors, but the driving mechanisms remain partially understood. Here we identify an early response to nerve injury controlled by histone deacetylase 2 (HDAC2), which coordinates the action of other chromatin-remodelling enzymes to induce the upregulation of Oct6, a key transcription factor for SC development. Inactivating this mechanism using mouse genetics allows earlier conversion into repair cells and leads to faster axonal regrowth, but impairs remyelination. Consistently, short-term HDAC1/2 inhibitor treatment early after lesion accelerates functional recovery and enhances regeneration, thereby identifying a new therapeutic strategy to improve PNS regeneration after lesion.

Date: 2017
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms14272

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DOI: 10.1038/ncomms14272

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