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Schwann cell release of p11 induces sensory neuron hyperactivity in Fabry disease. | LitMetric

AI Article Synopsis

  • - Patients with Fabry disease experience severe pain and nerve issues, and the specific causes behind this pain have not been clearly identified.
  • - Research using a genetic rat model reveals that altered communication between Schwann cells and sensory neurons leads to increased sensitivity and activity in sensory neurons.
  • - The study identifies the protein p11 (S100-A10) released by Schwann cells as a key factor that promotes hyperexcitability in sensory neurons, suggesting a potential target for treatment strategies.

Article Abstract

Patients with Fabry disease suffer from chronic debilitating pain and peripheral sensory neuropathy with minimal treatment options, but the cellular drivers of this pain are unknown. Here, we propose a novel mechanism by which altered signaling between Schwann cells and sensory neurons underlies the peripheral sensory nerve dysfunction we observe in a genetic rat model of Fabry disease. Using and electrophysiological recordings, we demonstrate that Fabry rat sensory neurons exhibit pronounced hyperexcitability. Schwann cells likely contribute to this finding as application of mediators released from cultured Fabry Schwann cells induces spontaneous activity and hyperexcitability in naïve sensory neurons. We examined putative algogenic mediators using proteomic analysis and found that Fabry Schwann cells release elevated levels of the protein p11 (S100-A10) which induces sensory neuron hyperexcitability. Removal of p11 from Fabry Schwann cell media causes hyperpolarization of neuronal resting membrane potential, indicating that p11 contributes to the excessive neuronal excitability caused by Fabry Schwann cells. These findings demonstrate that rats with Fabry disease exhibit sensory neuron hyperexcitability caused in part by Schwann cell release of the protein p11.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10245981PMC
http://dx.doi.org/10.1101/2023.05.26.542493DOI Listing

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