What is it about?
Spinal cord injury in mammals causes devastating conditions because there are currently no effective treatments to repair damaged neural circuits. However, deep within the spinal cord, ependymal cells react to injury by producing new cells that help restrict the damage. Manipulating these latent stem cells represents a promising strategy to improve healing.
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Why is it important?
To unlock the potential of the ependyma for repair, we must better understand the mechanisms that reactivate these dormant, progenitor-like cells. We focused on connexins (Cxs)—proteins that form channels for intercellular communication—because they are known regulators of stem cell biology. Indeed, ependymal cells express Cx43 under normal conditions and Cx26 only after injury. We found that Cx26 is critical for the proliferative response of ependymal cells to injury. Deleting Cx26 reduced this response, which increased the extent of the lesion due to impaired healing. On the other hand, Cx43 plays a key role in the communication of calcium signals between ependymal cells induced by the activation of purinergic P2X7 receptors. Our study is important because revealed that Cxs are relevant targets to manipulate the ependymal stem cell niche and achieve better healing after spinal cord injury.
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This page is a summary of: Connexins are essential for the contribution of latent progenitors to healing after spinal cord injury, Proceedings of the National Academy of Sciences, October 2026, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.2605647123.
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