• Mayara Vieira Mundim, Laura Nicoleti Zamproni, Agnes Araújo Sardinha Pinto, Layla Testa Galindo, André Machado Xavier, Isaias Glezer, and Marimélia Porcionatto.
• Department of Biochemistry, Laboratory of Neurobiology, Escola Paulista de Medicina, Universidade Federal de São Paulo, Rua Pedro de Toledo, 669 - 3o andar, São Paulo, SP 04039-032, Brazil.
• Mol. Cell. Neurosci. 2019 Jan 1; 94: 1-10.

AbstractTraumatic brain injury is an important cause of global morbidity and mortality. After an initial injury, there is a cascade of cellular and molecular events that ultimately lead to cell death. Therapies aim to both counteract these mechanisms and replenish the lost cell population in order to improve recovery. The adult mammal brain has at least two neurogenic regions that maintain physiological functions: the subgranular zone of the dentate gyrus in the hippocampus, which produces neurons that integrate locally, and the subventricular zone (SVZ) adjacent to the lateral ventricles, which produces neuroblasts that migrate through the rostral migratory stream (RMS) to the olfactory bulbs. Brain injuries, as well as neurodegenerative diseases, induce the SVZ to respond by increasing cell proliferation and migration to the injured areas. Here we report that cells migrate from the SVZ and RMS to the injured cortex after traumatic brain injury in mice, and that the physiological RMS migration is not impaired. We also show that Prokineticin 2 (PROK2), a chemokine important for the olfactory bulb neurogenesis, expressed exclusively by cortical microglia in the cortex as early as 24 h after injury. We then show that administration of a PROK2 receptor antagonist decreases the number of SVZ cells that reach the injured cortex, while injection of recombinant PROK2 into the cortex of uninjured mice attracts SVZ cells. We also demonstrate that cells expressing PROK2 in vitro directionally attract SVZ cells. These data suggest that PROK2 could be utilized in regeneration efforts for the acutely injured mammalian cortex.Copyright © 2018. Published by Elsevier Inc.

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