All-trans retinoic acid induces differentiation of ducts and endocrine cells by mesenchymal/epithelial interactions in embryonic pancreas

Diabetes. 2003 Jan;52(1):76-84. doi: 10.2337/diabetes.52.1.76.

Abstract

Retinoids during the embryonic period act as a mesenchymal inducer in many organs, including kidney, lung, central nervous system, and gut. Retinoic acid (RA) demonstrates insulinotropic effects in adult pancreas, but only a limited study has elucidated its role in pancreatic organogenesis. In this study, we have analyzed the existence of RA-signaling machinery in embryonic pancreas and evaluated its role using in vitro tissue culture experiments. Here we show the presence of endogenous retinaldehyde dehydrogenase 2 (RALDH2), the most effective RA-synthesizing enzyme, RA-binding proteins, and RA receptors (RARs) in embryonic pancreatic tissue. RALDH2 is expressed exclusively in the mesenchyme. Exogenously added all-trans-retinoic acid (atRA) in tissue culture experiments stimulated differentiation of endocrine and duct cells and promoted apoptotic cell death of acinar tissue. Furthermore, we demonstrate that atRA upregulates the PDX-1 expression. Taken together, our data suggest that atRA-mediated mesenchymal/epithelial interactions play an important role in determining the cell fate of epithelial cells via regulation of the PDX-1 gene, leading to the proper formation of the endocrine versus exocrine component during pancreatic organogenesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / physiology
  • Cell Differentiation / drug effects
  • Culture Techniques / methods
  • Embryo, Mammalian / cytology
  • Embryo, Mammalian / drug effects
  • Embryo, Mammalian / physiology
  • Embryo, Mammalian / ultrastructure
  • Endocrine System / embryology*
  • Epithelium / embryology
  • Female
  • Gels
  • Homeodomain Proteins*
  • Male
  • Mesoderm / physiology
  • Mice
  • Mice, Inbred ICR
  • Microscopy, Electron
  • Pancreatic Ducts / embryology*
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins c-bcl-2*
  • Retinoids / metabolism
  • Trans-Activators / metabolism
  • Tretinoin / administration & dosage
  • Tretinoin / pharmacology*
  • bcl-2-Associated X Protein

Substances

  • Gels
  • Homeodomain Proteins
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Retinoids
  • Trans-Activators
  • bcl-2-Associated X Protein
  • pancreatic and duodenal homeobox 1 protein
  • Tretinoin