Dr Samuel Crossman; The Australian Regenerative Medicine Â鶹ÊÓƵ, Monash University
Unlike mammals, regenerative vertebrates such as zebrafish and salamanders display near-complete recovery from traumatic spinal cord injuries. This exquisite capacity for neural repair can be attributed in part to the reactivation of quiescent progenitor cells, which re-enter the cell cycle upon injury and serve as neural stem cells in order to replace lost and defective tissues. Despite their critical role in regeneration, surprisingly little is known about the precise molecular identity of these spinal progenitor cells and the signals that govern their proliferation.
Here, I will present our work on a recently identified population of ciliated cells in the zebrafish spinal cord that detect mechanical changes in the injury microenvironment and orchestrate proliferation in the regenerating spinal cord. We find that spinal cord injuries initiate a local inflammatory response that triggers an increase in cerebrospinal fluid (CSF) circulation. This increase in CSF flow deforms mechanosensitive immotile cilia within the progenitor domain, resulting in an influx of calcium ions that is required for injury-induced proliferation to occur. Our results identify calcium as a central regulator of neural stem cell activity and highlight a previously uncharacterised role for mechanosensitive immotile cilia in the regenerating CNS.
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