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Peer-reviewedCC BY-NC-ND 4.0Proceedings of the National Academy of Sciences of the United States of America

Connexins are essential for the contribution of latent progenitors to healing after spinal cord injury

  • María Victoria Falco1
  • Gabriela Fabbiani1
  • Daniel Prieto1
  • Mateo Vidal1
  • Milagros Benítez1
  • María Inés Rehermann1
  • María Constanza Silvera1
  • Renata Simeone1
  • Federico F. Trigo2
  • Raúl E. Russo1
  1. 1Departamento de Neurofisiología Celular y Molecular, División Neurociencias, Instituto de Investigaciones Biológicas Clemente Estable, Montevideo CP11600, Uruguay
  2. 2Departamento de Señalización Neuronal y Glial, División Neurociencias, Instituto de Investigaciones Biológicas Clemente Estable, Montevideo CP11600, Uruguay
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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 signaling in the reactivation of ependymal cells. However, direct evidence of the involvement of these Cxs in the reactivation of the ependymal stem cell niche is lacking. Here, we aim to explore the role of Cx26 and Cx43 in the response of ependymal cells to injury by means of specific genetic deletion. We find that Cx26 is critical for the proliferative response of ependymal cells to injury. The reduced response of ependymal cells by Cx26 deletion increased the extension of the lesion because of impaired healing resulting from a weak contribution of the ependymal stem cell niche. On the other hand, Cx43—via gap junction coupling and hemichannels—plays a key role in the communication of Ca2+ signals between ependymal cells induced by activation of P2X7 receptors. Our data show that Cxs are relevant targets to manipulate the ependymal stem cell niche to achieve better healing after spinal cord injury.

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Cite

BibTeXRIS
BibTeX
@article{falco2026connexins,
  title = {{Connexins are essential for the contribution of latent progenitors to healing after spinal cord injury}},
  author = {María Victoria Falco and Gabriela Fabbiani and Daniel Prieto and Mateo Vidal and Milagros Benítez and María Inés Rehermann and María Constanza Silvera and Renata Simeone and Federico F. Trigo and Raúl E. Russo},
  journal = {Proceedings of the National Academy of Sciences of the United States of America},
  year = {2026},
  month = oct,
  doi = {10.1073/pnas.2605647123},
  url = {https://doi.org/10.1073/pnas.2605647123},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - Connexins are essential for the contribution of latent progenitors to healing after spinal cord injury
AU  - María Victoria Falco
AU  - Gabriela Fabbiani
AU  - Daniel Prieto
AU  - Mateo Vidal
AU  - Milagros Benítez
AU  - María Inés Rehermann
AU  - María Constanza Silvera
AU  - Renata Simeone
AU  - Federico F. Trigo
AU  - Raúl E. Russo
PY  - 2026
DA  - 2026/10/20
JO  - Proceedings of the National Academy of Sciences of the United States of America
DO  - 10.1073/pnas.2605647123
UR  - https://doi.org/10.1073/pnas.2605647123
AB  - 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 signaling in the reactivation of ependymal cells. However, direct evidence of the involvement of these Cxs in the reactivation of the ependymal stem cell niche is lacking. Here, we aim to explore the role of Cx26 and Cx43 in the response of ependymal cells to injury by means of specific genetic deletion. We find that Cx26 is critical for the proliferative response of ependymal cells to injury. The reduced response of ependymal cells by Cx26 deletion increased the extension of the lesion because of impaired healing resulting from a weak contribution of the ependymal stem cell niche. On the other hand, Cx43—via gap junction coupling and hemichannels—plays a key role in the communication of Ca2+ signals between ependymal cells induced by activation of P2X7 receptors. Our data show that Cxs are relevant targets to manipulate the ependymal stem cell niche to achieve better healing after spinal cord injury.
SN  - 0027-8424
SN  - 1091-6490
ER  -