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All-trans retinoic acid suppresses exocrine differentiation and branching morphogenesis in the embryonic pancreas

Chia-Ning Shen1, Anita Marguerie, Chiao-Yun Chien

  • 1Centre for Regenerative Medicine, Department of Biology and Biochemistry, University of Bath, Bath BA2 7AY, UK.

Differentiation; Research in Biological Diversity
|January 25, 2007
PubMed

Insights

Retinoic acid (RA) inhibits mouse embryonic pancreas development by suppressing branching and exocrine differentiation while promoting premature endocrine cell formation. Fibroblast growth factor (FGF)-10 partially rescues these effects via FGF receptor 2-IIIb.

Area of Science:

  • Developmental biology
  • Endocrinology
  • Molecular biology

Background:

  • Retinoic acid (RA) signaling is crucial for early pancreatic development in amphibians but its role in mammalian pancreatic differentiation remains unclear.
  • Understanding RA's impact on mammalian pancreas development is vital for regenerative medicine and treating pancreatic diseases.

Purpose of the Study:

  • To investigate the effects of all-trans retinoic acid (atRA) on mouse embryonic pancreatic differentiation.
  • To elucidate the underlying mechanisms of atRA-induced changes in pancreatic development.
  • To explore the potential role of fibroblast growth factor (FGF)-10 in modulating these effects.

Main Methods:

  • Organotypic culture of mouse embryonic pancreas with atRA treatment.
  • Analysis of branching morphogenesis and exocrine/endocrine cell differentiation markers.
  • Investigation of gene expression (Pdx1) and apoptosis.
  • FGF-10 treatment and assessment in wild-type and FGF receptor mutant mice.

Main Results:

  • atRA suppressed branching morphogenesis and exocrine differentiation.
  • Premature formation of endocrine cell clusters was observed, linked to early Pdx1 expression.
  • RA's suppressive effects on exocrine differentiation involved laminin up-regulation and enhanced apoptosis.
  • FGF-10 partially rescued apoptosis and exocrine differentiation, mediated through FGF receptor 2-IIIb.

Conclusions:

  • Retinoic acid significantly impacts mouse embryonic pancreatic differentiation, inhibiting key developmental processes.
  • RA's effects are mediated through modulation of Pdx1 expression, extracellular matrix components, and apoptosis.
  • FGF-10 acts through FGF receptor 2-IIIb to counteract some of RA's inhibitory effects on pancreatic development.

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