Connexins are essential for the contribution of latent progenitors to self-repair after spinal cord injury

Abstract

Gap junctions are important regulators of the biology of neural stem cells. Both in vertebrates with regenerative abilities and neonatal rodents, ependymal cells communicate via connexin (Cx) 43 and Cx26. Gap junction coupling and Cx26 are down-regulated as the ependyma becomes quiescent in adulthood, but injury overrules this developmental down-regulation suggesting a role for Cx signalling in the reactivation of ependymal cells. Here, we aim to explore the role of Cx26 and Cx43 in the response of ependymal cells to injury. We find that Cx26 is critical for the proliferative response to injury and thereby scar formation. Cx43 plays a key role in the communication between ependymal cells of Ca2+ signals induced by activation of P2X7 receptors that trigger downstream events. Our data show that Cxs are relevant targets to manipulate the ependymal stem cell niche to achieve a better self-repair after spinal cord injury.