Abstract
Peripheral neuropathy is a pathological pain state occurring many population caused by anti-cancer drug treatment, lesion or disease of the somatosensory system. An important mechanistic aspect of peripheral neuropathy is the reciprocal communication between the Schwann cells with the peripheral nervous systems.
Promoting our research on chemotherapy-induced peripheral neuropathy (CIPN), we found that paclitaxel reduces myelin-forming Schwann cells by promoting their dedifferentiation. Furthermore, paclitaxel treatment increased secretory protein galectin-3 in Schwann cells within the sciatic nerve of paclitaxel-related CIPN model mice. Using this mouse model, we further demonstrated that Schwann cell-derived galectin-3 plays a pro-nociceptive role via macrophage infiltration in the pathogenesis of taxane-related CIPN.
On the other hand, there are not many in vitro experimental systems optimized for analyzing the peripheral nervous system (PNS), which aims to investigate the interaction between Schwann cells and sensory nerves that underlies the onset of peripheral neuropathy. To further advance the study of peripheral neuropathy, we developed a novel sensory nerve organoid derived from rat embryonic dorsal root ganglion.
In this presentation, I would like to present our series of new findings on the mechanisms of CIPN pathogenesis and further discuss the potential and future prospects of novel organoids in peripheral nerve research.
