Sodium phenylbutyrate inhibits Schwann cell inflammation via HDAC and NFκB to promote axonal regeneration and remyelination.

ABSTRACT:

Background

Epigenetic regulation by histone deacetylases (HDACs) in Schwann cells (SCs) after injury facilitates them to undergo de- and redifferentiation processes necessary to support various stages of nerve repair. Although de-differentiation activates the synthesis and secretion of inflammatory cytokines by SCs to initiate an immune response during nerve repair, changes in either the timing or duration of prolonged inflammation mediated by SCs can affect later processes associated with repair and regeneration. Limited studies have investigated the regulatory processes through which HDACs in SCs control inflammatory cytokines to provide a favorable environment for peripheral nerve regeneration.

Methods

We employed the HDAC inhibitor (HDACi) sodium phenylbutyrate (PBA) to

SUBMITTER: Yadav A 

PROVIDER: S-EPMC8520633 | biostudies-literature | 2021 Oct

REPOSITORIES: biostudies-literature