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Metabolism fuels intestinal stem cell renewal. Paneth cells provide lactate to Lgr5+ stem cells, supporting mitochondrial function and differentiation via reactive oxygen species signaling.

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Area of Science:

  • Gastroenterology
  • Cell Biology
  • Metabolism

Background:

  • The small intestinal epithelium undergoes rapid self-renewal, driven by Lgr5+ stem cells located at the crypt base.
  • While signaling pathways regulating stem cell function are known, the metabolic contributions to epithelial homeostasis remain largely unexplored.

Purpose of the Study:

  • To investigate the distinct metabolic programs of intestinal stem cells and Paneth cells.
  • To elucidate the role of cellular metabolism in maintaining intestinal epithelial homeostasis and stem cell function.

Main Methods:

  • Isolation of Lgr5+ CBCs and Paneth cells from mouse small intestine.
  • Assessment of mitochondrial activity and glycolysis.
  • Inhibition of mitochondrial activity and glycolysis.
  • Organoid formation assays.
  • Analysis of reactive oxygen species signaling and p38 MAPK activation.

Main Results:

  • Lgr5+ CBCs exhibit higher mitochondrial activity compared to Paneth cells.
  • Inhibition of mitochondrial activity in Lgr5+ CBCs impairs stem cell function.
  • Inhibition of glycolysis in Paneth cells also affects stem cell function.
  • Paneth cells supply lactate to Lgr5+ CBCs, supporting their oxidative phosphorylation.
  • Oxidative phosphorylation activates p38 MAPK via ROS signaling, promoting crypt maturation.

Conclusions:

  • Distinct metabolic programs in Lgr5+ CBCs and Paneth cells are crucial for intestinal stem cell function.
  • Paneth cell-derived lactate supports Lgr5+ CBC metabolism and differentiation.
  • Mitochondrial oxidative phosphorylation and ROS signaling are key drivers of cellular differentiation in the intestinal crypt.