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Regulation of pancreas development by hedgehog signaling

M Hebrok1, S K Kim, B St Jacques

  • 1Department of Molecular and Cellular Biology and Howard Hughes Medical Institute, Harvard University, Cambridge, MA 02138, USA.

Development (Cambridge, England)
|October 25, 2000
PubMed

Insights

Indian hedgehog (Ihh) and Sonic hedgehog (Shh) signaling regulate pancreas development. Ihh inactivation causes annular pancreas, while Shh and Ihh pathway alterations affect pancreas mass and endocrine cell numbers, impacting glucose homeostasis.

Area of Science:

  • Developmental biology
  • Endocrinology
  • Genetics

Background:

  • Pancreas organogenesis relies on signaling pathways controlling morphogenesis and differentiation.
  • Activin (a TGF-β molecule) promotes pancreas development by inhibiting Sonic hedgehog (Shh).
  • Shh antagonizes pancreas development.

Purpose of the Study:

  • To investigate the roles of Indian hedgehog (Ihh) and Patched 1 (Ptc1) in pancreas development.
  • To understand the impact of hedgehog signaling on pancreatic morphogenesis and cell differentiation.

Main Methods:

  • Targeted gene inactivation of Ihh in mice.
  • Analysis of Shh and Ihh double mutants.
  • Study of Patched 1 (Ptc1) mutations in mice.
  • Assessment of pancreatic morphology, mass, and endocrine cell numbers.
  • Evaluation of glucose homeostasis.

Main Results:

  • Ihh inactivation in mice led to ectopic ventral pancreatic branching, forming an annular pancreas.
  • Shh/Ihh mutants exhibited increased pancreas mass and endocrine cell numbers.
  • Ptc1 mutations reduced pancreatic gene expression and impaired glucose homeostasis.
  • Hedgehog signaling molecules regulate islet cell development, pancreatic mass, and morphogenesis.

Conclusions:

  • Hedgehog signaling pathways, including Ihh and Shh, are critical regulators of embryonic pancreas development.
  • Dysregulation of hedgehog signaling can result in congenital pancreatic malformations like annular pancreas.
  • Aberrant hedgehog signaling is linked to impaired glucose homeostasis and potential diabetes development.

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