Negative cell cycle regulation by calcineurin is necessary for proper beta cell regeneration in zebrafish

Elife. 2024 Oct 9:12:RP88813. doi: 10.7554/eLife.88813.

Abstract

Stimulation of pancreatic beta cell regeneration could be a therapeutic lead to treat diabetes. Unlike humans, the zebrafish can efficiently regenerate beta cells, notably from ductal pancreatic progenitors. To gain insight into the molecular pathways involved in this process, we established the transcriptomic profile of the ductal cells after beta cell ablation in the adult zebrafish. These data highlighted the protein phosphatase calcineurin (CaN) as a new potential modulator of beta cell regeneration. We showed that CaN overexpression abolished the regenerative response, leading to glycemia dysregulation. On the opposite, CaN inhibition increased ductal cell proliferation and subsequent beta cell regeneration. Interestingly, the enhanced proliferation of the progenitors was paradoxically coupled with their exhaustion. This suggests that the proliferating progenitors are next entering in differentiation. CaN appears as a guardian which prevents an excessive progenitor proliferation to preserve the pool of progenitors. Altogether, our findings reveal CaN as a key player in the balance between proliferation and differentiation to enable a proper beta cell regeneration.

Keywords: beta cell; developmental biology; progenitor; regeneration; regenerative medicine; stem cells; zebrafish.

MeSH terms

  • Animals
  • Calcineurin* / genetics
  • Calcineurin* / metabolism
  • Cell Cycle
  • Cell Differentiation
  • Cell Proliferation*
  • Gene Expression Profiling
  • Insulin-Secreting Cells* / metabolism
  • Insulin-Secreting Cells* / physiology
  • Regeneration*
  • Zebrafish Proteins / genetics
  • Zebrafish Proteins / metabolism
  • Zebrafish*

Substances

  • Calcineurin
  • Zebrafish Proteins

Associated data

  • GEO/GSE212124

Grants and funding

The funders had no role in study design, data collection, and interpretation, or the decision to submit the work for publication.