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Phosphatidylinositol 3-Kinase Signaling Enhances Intestinal Crypt Epithelial Cell Recovery after Radiation.

Evan B Lynch1, Neeraj Kapur2, Tatiana Goretsky2

  • 1Department of Microbiology, Immunology and Molecular Genetics, University of Kentucky, Lexington, Kentucky; Division of Plastic Surgery, Department of Surgery, University of Kentucky, Lexington, Kentucky; Division of Digestive Diseases and Nutrition, Department of Medicine, University of Kentucky, Lexington, Kentucky.

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Phosphatidylinositol 3-kinase (PI3K) signaling enhances intestinal stem cell (ISC) recovery after radiation by increasing mitochondrial reactive oxygen species. This suggests PI3K activation could improve mucosal healing in patients with radiation injury.

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Area of Science:

  • Gastroenterology and Molecular Biology
  • Cellular signaling in tissue repair
  • Radiation biology

Background:

  • Intestinal stem cells (ISCs) regulate tissue homeostasis through self-renewal and differentiation.
  • Radiation exposure disrupts the intestinal epithelium, necessitating effective repair mechanisms.
  • The role of phosphatidylinositol 3-kinase (PI3K) signaling in ISC response to radiation injury requires further elucidation.

Purpose of the Study:

  • To investigate the function of PI3K signaling in intestinal stem cell (ISC) responses to radiation.
  • To determine the impact of PI3K pathway activation on intestinal epithelial cell (IEC) survival and recovery post-irradiation.
  • To explore the therapeutic potential of modulating PI3K signaling for radiation-induced mucosal injury.

Main Methods:

  • Utilized Villin-Cre pik3r1lox/lox (p85ΔIEC) mice and p85α-deficient human enteroids (shp85α) to study PI3K signaling.
  • Administered lethal whole-body irradiation to mice to assess PI3K-mediated survival.
  • Examined rectal biopsies from patients with radiation proctitis using immunohistochemistry for PI3K/Akt and Wnt targets.

Main Results:

  • Enhanced PI3K signaling in mice and enteroids increased levels of phosphorylated Akt, survivin, cyclin D1, and Wnt/ISC targets.
  • PI3K activation reduced Lgr5+ ISC populations but expanded Axin2+ progenitor cells, indicating altered stem cell dynamics.
  • Increased PI3K signaling led to enhanced mitochondrial respiration and reactive oxygen species (ROS) generation in IECs.
  • Survivin expression correlated with radiation injury severity in patients.

Conclusions:

  • PI3K signaling promotes ISC activation and enhances IEC recovery from radiation injury by increasing mitochondrial ROS generation.
  • Modulating PI3K signaling and mitochondrial respiration presents a potential therapeutic strategy for improving mucosal healing in patients suffering from radiation-induced injury.