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Related Concept Videos

CRISPR01:59

CRISPR

Genome editing technologies allow scientists to modify an organism’s DNA via the addition, removal, or rearrangement of genetic material at specific genomic locations. These types of techniques could potentially be used to cure genetic disorders such as hemophilia and sickle cell anemia. One popular and widely used DNA-editing research tool that could lead to safe and effective cures for genetic disorders is the CRISPR-Cas9 system. CRISPR-Cas9 stands for Clustered Regularly Interspaced Short...
CRISPR01:59

CRISPR

Genome editing technologies allow scientists to modify an organism’s DNA via the addition, removal, or rearrangement of genetic material at specific genomic locations. These types of techniques could potentially be used to cure genetic disorders such as hemophilia and sickle cell anemia. One popular and widely used DNA-editing research tool that could lead to safe and effective cures for genetic disorders is the CRISPR-Cas9 system. CRISPR-Cas9 stands for Clustered Regularly Interspaced Short...

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Bidirectional CRISPR screens decode a GLIS3-dependent fibrotic cell circuit.

Vladislav Pokatayev1,2,3, Alok Jaiswal2,3, Angela R Shih4

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Researchers identified a key immune-stromal cell circuit driving fibrosis in inflammatory bowel disease. This pathway involves inflammation-associated fibroblasts regulated by the transcription factor GLIS3, offering potential therapeutic targets for chronic colitis.

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Area of Science:

  • Immunology
  • Gastroenterology
  • Cell Biology

Background:

  • Stromal cells coordinate immune responses and tissue homeostasis.
  • Chronic inflammation can lead to fibrosis, a common complication in inflammatory bowel disease (IBD).
  • Fibrosis and treatment-refractory disease in IBD are linked to stromal fibroblasts, but their activation mechanisms are unclear.

Purpose of the Study:

  • To elucidate the mechanisms of stromal fibroblast activation in inflammatory bowel disease.
  • To identify key regulators of the inflammation-fibrosis cycle in the intestine.
  • To explore the potential of targeting this pathway for therapeutic benefit.

Main Methods:

  • Integrative single-cell and spatial profiling of intestinal tissues from IBD patients.
  • Genome-wide CRISPR screens (knockout and activation) to identify regulatory networks.
  • Analysis of GLIS3 gene expression in patient biopsies and fibroblast-specific Glis3 deletion in mouse models of colitis.

Main Results:

  • A pathological cell nexus centered on inflammation-associated fibroblasts was identified.
  • These fibroblasts are induced by proinflammatory macrophages and produce the profibrotic cytokine IL-11.
  • The transcription factor GLIS3 was identified as a key regulator of inflammatory and fibrotic gene expression.
  • GLIS3 expression levels correlate with ulcerative colitis disease severity.
  • Fibroblast-specific Glis3 deletion in mice ameliorated chronic colitis pathology.

Conclusions:

  • A critical immune-stromal cell circuit, involving GLIS3-regulated fibroblasts, drives the inflammation-fibrosis cycle in IBD.
  • This pathway represents a potential therapeutic target for inflammatory bowel disease and associated fibrosis.
  • GLIS3 serves as a biomarker for disease severity in ulcerative colitis.