Calcium-dependent neuroepithelial contractions expel damaged cells from the developing brain
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Updated: Apr 20, 2026

Double In Utero Electroporation to Target Temporally and Spatially Separated Cell Populations
Published on: June 14, 2020
Leah Herrgen1, Oliver P Voss1, Colin J Akerman1
1Department of Pharmacology, University of Oxford, Mansfield Road, Oxford OX1 3QT, UK.
Abstract:
Both developing and adult organisms need efficient strategies for wound repair. In adult mammals, wounding triggers an inflammatory response that can exacerbate tissue injury and lead to scarring. In contrast, embryonic wounds heal quickly and with minimal inflammation, but how this is achieved remains incompletely understood. Using in vivo imaging in the developing brain of Xenopus laevis, we show that ATP release from damaged cells and subsequent activation of purinergic receptors induce long-range calcium waves in neural progenitor cells. Cytoskeletal reorganization and activation of the actomyosin contractile machinery in a Rho kinase-dependent manner then lead to rapid and pronounced apical-basal contractions of the neuroepithelium. These contractions drive the expulsion of damaged cells into the brain ventricle within seconds. Successful cell expulsion prevents the death of nearby cells and an exacerbation of the injury. Cell expulsion through neuroepithelial contraction represents a mechanism for rapid wound healing in the developing brain.
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