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The intestinal epithelial lining rapidly renews every 4 to 5 days. The renewal is facilitated by intestinal stem cells (ISCs) located at the base of the crypt– a gland located at the bottom of each villus. ISCs divide asymmetrically to form new stem cells and progenitor daughter cells. The daughter cells are called transit-amplifying (TA) cells which move upwards along the crypt and either differentiate into absorptive cells– the enterocytes or secretory cells– including the...
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Stem cells are undifferentiated cells that divide and produce more stem cells or progenitor cells that differentiate into mature, specialized cell types. All the cells in the body are generated from stem cells in the early embryo, but small populations of stem cells are also present in many adult tissues including the bone marrow, brain, skin, and gut. These adult stem cells typically produce the various cell types found in that tissue—to replace cells that are damaged or to continuously...
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DR3 Regulates Intestinal Epithelial Homeostasis and Regeneration After Intestinal Barrier Injury.

Yosuke Shimodaira1, Shyam K More1, Hussein Hamade1

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Death receptor 3 (DR3) plays a crucial role in maintaining intestinal epithelial barrier function and promoting tissue repair after injury. Its absence exacerbates intestinal inflammation and impairs regeneration.

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Area of Science:

  • Gastroenterology
  • Immunology
  • Cell Biology

Background:

  • Tumor necrosis factor-like protein 1A (TL1A) and its receptor, death receptor 3 (DR3), are implicated in inflammatory bowel diseases.
  • The precise role of DR3 in intestinal epithelial cells (IECs) during homeostasis, injury, and regeneration remains unclear.

Purpose of the Study:

  • To investigate the function of DR3 expressed by IECs in the context of intestinal homeostasis, tissue injury, and regeneration.

Main Methods:

  • Utilized dextran sulfate sodium (DSS)-induced colitis models in wild-type, Tl1a knockout (Tl1a-/-), and Dr3 knockout (Dr3-/-) mice.
  • Generated IEC-specific DR3 knockout mice (Dr3ΔIEC) to assess epithelial barrier repair and inflammation.
  • Assessed in vivo intestinal permeability, IEC proliferation, and ex vivo regenerative potential using organoids.

Main Results:

  • Dr3-/- mice exhibited more severe colitis and impaired IEC regeneration compared to wild-type mice.
  • DR3 deficiency led to increased homeostatic IEC proliferation but blunted regeneration, altered tight junction protein expression, and increased intestinal permeability.
  • IEC-specific DR3 deletion (Dr3ΔIEC) recapitulated these findings, showing impaired repair and increased bacterial translocation during colitis.

Conclusions:

  • DR3 has a novel, essential function in maintaining IEC homeostasis and facilitating post-injury regeneration.
  • This function of DR3 in IECs is independent of its known roles in innate lymphoid cells and T-helper cells.