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LSD1 represses a neonatal/reparative gene program in adult intestinal epithelium

Rosalie T Zwiggelaar1, Håvard T Lindholm1, Madeleine Fosslie2

  • 1CEMIR-Centre of Molecular Inflammation Research, Department of Clinical and Molecular Medicine, NTNU-Norwegian University of Science and Technology, 7491 Trondheim, Norway.

Science Advances
|September 12, 2020
PubMed

Insights

Lysine-specific demethylase 1A (LSD1) is essential for Paneth cell development in the neonatal intestine. LSD1 inhibition enhances intestinal epithelial regeneration after injury, offering a potential therapeutic target.

Area of Science:

  • Gastroenterology
  • Developmental Biology
  • Epigenetics

Background:

  • Intestinal epithelial homeostasis relies on adult stem cells and Paneth cells, which emerge postnatally.
  • Neonatal intestinal development requires precise regulation of epithelial cell differentiation.

Purpose of the Study:

  • To identify epigenetic regulators of neonatal intestinal epithelial development.
  • To investigate the role of lysine-specific demethylase 1A (KDM1A/LSD1) in Paneth cell differentiation.

Main Methods:

  • Utilized Paneth cell-skewed organoid cultures with epigenetic modifier inhibitors.
  • Tested Lsd1-deficient crypts for organoid formation and regenerative capacity.
  • Analyzed gene expression profiles in Lsd1-deficient epithelium.

Main Results:

  • Lysine-specific demethylase 1A (LSD1) is crucial for Paneth cell differentiation.
  • LSD1 deficiency allows Wnt-independent organoid formation and represses fetal/neonatal gene expression.
  • LSD1-deficient epithelium exhibits enhanced regenerative capacity after irradiation injury.

Conclusions:

  • LSD1 is a key regulator of neonatal intestinal development.
  • Targeting LSD1 can reprogram intestinal epithelium towards a reparative state, suggesting therapeutic potential for regenerative medicine.

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