1. Endothelin/endothelin-B receptor signals regulate ventricle-directed interkinetic nuclear migration of cerebral cortical neural progenitors.
- Author
-
Nishikawa K, Ayukawa K, Hara Y, Wada K, and Aoki S
- Subjects
- Animals, Cell Nucleus ultrastructure, Cells, Cultured, Cerebral Cortex cytology, Endothelin B Receptor Antagonists, Mice, Mice, Inbred C57BL, Neural Stem Cells cytology, Organ Culture Techniques, Receptor, Endothelin B agonists, Cell Movement physiology, Cell Nucleus metabolism, Cerebral Cortex embryology, Endothelins physiology, Neural Stem Cells metabolism, Receptor, Endothelin B physiology
- Abstract
We determined the expression profile of ∼300 G protein-coupled receptors (GPCRs) in embryonic cortical neural progenitor cells (NPCs) and identified a number of highly expressed GPCRs, among which endothelin-B receptor (ET(B)-R) was expressed at the highest level. We also revealed that endothelins (ETs) were predominantly expressed in CD31-positive endothelial cells of the embryonic cerebral cortex. Activation of ET(B)-R induced NPC assembly in vitro by promoting fibronectin-dependent-motility and N-cadherin-associated cell contact. NPC assembly also required a Rho-family GTPase(s) and phosphatidylinositol-3-kinase. In the embryonic cerebral cortex, a specific ET(B)-R agonist, IRL-1620, accelerated interkinetic nuclear migration (INM) of NPCs toward the ventricular wall (VW) ex vivo. Conversely, a specific ET(B)-R antagonist, BQ788, slowed INM, thereby inducing mislocalization of phospho-histone H3-positive M-phase nuclei in the ventricular zone (VZ) and decreasing the number of Tuj1-positive newborn neurons. Our results suggest that ET(B)-R-mediated assembly signals drive INM that precedes neurogenesis., (Copyright © 2010 Elsevier Ltd. All rights reserved.)
- Published
- 2011
- Full Text
- View/download PDF