Abstract
The adult mammalian brain contains neural stem cells (NSCs) that generate neurons and glial cells throughout the lifetime of an organism. NSCs reside in at least two germinal epithelium regions of the adult brain, the subventricular zone (SVZ) of the lateral ventricles and the subgranular zone of the hippocampus. Newborn neurons incorporate into the existing functional networks and play important innate and adaptive roles in cognition, behavior and tissue repair1,2. The identity of particular neural stem cells that generate different classes of neurons and glia, as well as the molecular mechanisms that governs this process in vivo, is a subject of extensive research and debate. Epidermal Growth Factor Receptor (EGFR) activation is one of the most important pathways controlling neural stem cell number and self-renewal3,4. On the other hand, the Shaker-type delayed rectifier K+ channel Kv1.3 functions during cell proliferation, differentiation and migration in many cell types5. This channel is expressed in brain progenitor cells where participates in modulating their final fate. This review summarizes the major findings concerning Kv1.3 and neural stem cell modulation, emphasizing the combination of Kv1.3 with EGFR as promising pharmacological targets against autoimmune neuro-degenerative diseases.
Highlights
Martínez-Mármol R, Salla-Martret M, Sastre D, Estadella I, Felipe A
Reduction of Epidermal Growth Factor Receptor (EGFR) signaling in NG2-expressing progenitors decreases subventricular zone (SVZ)-to-lesion migration of NG2+ cells and the subsequent oligodendrogenesis and remyelination rates
This demonstrates that the NG2+ cell response in the SVZ and the subsequent differentiation of these cells after focal demyelination are dependent upon EGFR signaling[34]
Summary
Martínez-Mármol R, Salla-Martret M, Sastre D, Estadella I, Felipe A. Our results are consistent with the facts that pSVZ contains progenitor cells that generate glial cells[18,19] and that Kv1.3 is functionally expressed in OPCs from the SVZ. Consistent with these studies, granzyme B (GrB) released by T-cells increases the expression of Kv1.3 within NPCs and hampers NPC proliferation and neuronal differentiation.
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