Calcium-dependent neuroepithelial contractions expel damaged cells from the developing brain

• Published in: Developmental cell Vol. 31; no. 5; pp. 599 - 613
• Main Authors: Herrgen, Leah, Voss, Oliver P., Akerman, Colin J.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 08-12-2014
• Subjects: Actomyosin - metabolism; Animals; Brain - cytology; Brain - growth & development; Brain - metabolism; Calcium - metabolism; Cell Death - physiology; Epithelium - metabolism; Epithelium - pathology; Wound Healing - physiology; Xenopus laevis - growth & development; Xenopus laevis - metabolism
• ISSN: 1534-5807; 1878-1551
• DOI: 10.1016/j.devcel.2014.10.012

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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ATP release from damaged cells triggers calcium waves in the developing brainCalcium waves are associated with apical-basal contractions of the neuroepitheliumThese actomyosin-mediated contractions lead to rapid expulsion of necrotic cellsRapid expulsion protects the developing brain from an exacerbation of the injury