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Neurog3 misexpression unravels mouse pancreatic ductal cell plasticity

Author

Listed:
  • Andhira Vieira
  • Bastien Vergoni
  • Monica Courtney
  • Noémie Druelle
  • Elisabet Gjernes
  • Biljana Hadzic
  • Fabio Avolio
  • Tiziana Napolitano
  • Sergi Navarro Sanz
  • Ahmed Mansouri
  • Patrick Collombat

Abstract

In the context of type 1 diabetes research and the development of insulin-producing β-cell replacement strategies, whether pancreatic ductal cells retain their developmental capability to adopt an endocrine cell identity remains debated, most likely due to the diversity of models employed to induce pancreatic regeneration. In this work, rather than injuring the pancreas, we developed a mouse model allowing the inducible misexpression of the proendocrine gene Neurog3 in ductal cells in vivo. These animals developed a progressive islet hypertrophy attributed to a proportional increase in all endocrine cell populations. Lineage tracing experiments indicated a continuous neo-generation of endocrine cells exhibiting a ductal ontogeny. Interestingly, the resulting supplementary β-like cells were found to be functional. Based on these findings, we suggest that ductal cells could represent a renewable source of new β-like cells and that strategies aiming at controlling the expression of Neurog3, or of its molecular targets/co-factors, may pave new avenues for the improved treatments of diabetes.

Suggested Citation

  • Andhira Vieira & Bastien Vergoni & Monica Courtney & Noémie Druelle & Elisabet Gjernes & Biljana Hadzic & Fabio Avolio & Tiziana Napolitano & Sergi Navarro Sanz & Ahmed Mansouri & Patrick Collombat, 2018. "Neurog3 misexpression unravels mouse pancreatic ductal cell plasticity," PLOS ONE, Public Library of Science, vol. 13(8), pages 1-22, August.
  • Handle: RePEc:plo:pone00:0201536
    DOI: 10.1371/journal.pone.0201536
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    References listed on IDEAS

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    1. Yuval Dor & Juliana Brown & Olga I. Martinez & Douglas A. Melton, 2004. "Adult pancreatic β-cells are formed by self-duplication rather than stem-cell differentiation," Nature, Nature, vol. 429(6987), pages 41-46, May.
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