Abstract

Schwann cells (SC) myelinate peripheral axons and orchestrate nerve regeneration after injury by switching between myelinating, proliferative and repair states. Evidence suggests that Botulinum Neurotoxin Type A (BoNT/A) influences SC biology, potentially supporting nerve repair and pain relief in peripheral neuropathic pain (PNP) models. However, BoNT/A receptor and target expression in human SC (hSC) remains poorly explored. Here, this translational gap was addressed by transcriptionally profiling genes encoding BoNT/A-relevant receptors and targets in primary hSC and testing whether paclitaxel evokes hSC phenotype plasticity in vitro based on changes in gene expression. Primary hSC were isolated, cultured, and treated with paclitaxel or vehicle, followed by RT-qPCR profiling of hSC markers and BoNT/A receptor/targets genes. Untreated hSC expressed moderate NGFR and S100β, with low MBP levels, suggesting a non-myelinating state profile. Transcripts encoding the BoNT/A receptor machinery (SV2A, SYT1) and the target SNAP25 were detectable at moderate levels. Paclitaxel induced changes in gene expression: SV2A and SYT1 decreased (up to two-fold), whereas SNAP25 and MBP increased, accompanied by reduced NGFR, indicating a shift toward a more differentiated transcriptional state. These data indicate hSC transcriptional plasticity in vitro and provide transcriptional evidence for the expression of BoNT/A-related molecular components in non-neuronal human cells.

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