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Related Concept Videos

Renewal of Intestinal Stem Cells01:23

Renewal of Intestinal Stem Cells

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 goblet,...
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

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Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal01:22

Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal

Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.

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Updated: Jun 20, 2026

In Vivo Augmentation of Gut-Homing Regulatory T Cell Induction
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Published on: January 22, 2020

Targeting CCDC90B restores intestinal stem cell function under hyperuricemic stress.

Xiuying Peng1, Moxuan Li2, Kaixuan Zeng2

  • 1Department of Gastroenterology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510630, China.

Stem Cell Reports
|June 18, 2026
PubMed
Summary

High uric acid levels impair intestinal stem cell function, disrupting the gut barrier. This occurs via CCDC90B binding, leading to inflammation and stem cell exhaustion, suggesting CCDC90B as a therapeutic target.

Keywords:
CCDC90Bhyperuricemiaintestinal organoidsintestinal stem cellspyroptosis

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Area of Science:

  • Gastroenterology
  • Molecular Biology
  • Immunology

Background:

  • Hyperuricemia (HUA) impacts various biological processes but its effects on the intestine are unclear.
  • Intestinal stem cells (ISCs) are crucial for maintaining epithelial integrity and regeneration.
  • Disruption of the intestinal barrier is linked to numerous gastrointestinal diseases.

Purpose of the Study:

  • To investigate the impact of hyperuricemia on intestinal barrier function.
  • To elucidate the underlying molecular mechanisms by which elevated uric acid affects intestinal stem cells.
  • To identify potential therapeutic targets for HUA-associated intestinal dysfunction.

Main Methods:

  • In vivo and in vitro models to study hyperuricemia effects on the intestine.
  • Mitochondrial protein analysis and reactive oxygen species (ROS) detection.
  • Assessment of NLRP3 inflammasome activation and pyroptosis.
  • Evaluation of intestinal stem cell function and epithelial regeneration.

Main Results:

  • Hyperuricemia impairs intestinal barrier function by affecting intestinal stem cell (ISC) function.
  • Elevated uric acid directly binds to CCDC90B, increasing mitochondrial ROS production.
  • This leads to NLRP3 inflammasome activation, pyroptosis, and ISC exhaustion.
  • Impaired ISC function results in reduced epithelial regeneration and compromised intestinal barrier integrity.

Conclusions:

  • Hyperuricemia disrupts intestinal barrier integrity through ISC dysfunction.
  • The mechanism involves uric acid binding to CCDC90B, causing oxidative stress and pyroptosis.
  • CCDC90B is identified as a key mediator and potential therapeutic target for HUA-related intestinal issues.