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Related Experiment Video

Updated: Jun 2, 2025

Effect of Hyaluronic Acid 35 kDa on an In Vitro Model of Preterm Small Intestinal Injury and Healing Using Enteroid-Derived Monolayers
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Rhamnogalacturonan promotes intestinal mucosal repair through increased cell migration.

Cristiane H Baggio1, Judie Shang1, Larissa L Périco1

  • 1Department of Physiology and Pharmacology, Calvin, Phoebe and Joan Snyder Institute for Chronic Diseases, University of Calgary, Calgary, Alberta, Canada.

American Journal of Physiology. Gastrointestinal and Liver Physiology
|January 17, 2025
PubMed
Summary
This summary is machine-generated.

Rhamnogalacturonan (RGal) promotes intestinal epithelial wound healing by enhancing cell migration via FAK, Src, PI3K, Rho, JNK, and NF-κB pathways. RGal also accelerated mucosal healing in mice with colitis.

Keywords:
DSS-induced colitiscell migrationdietary fiberepithelial wound healing

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A Novel In Vitro Wound Healing Assay to Evaluate Cell Migration
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A Novel In Vitro Wound Healing Assay to Evaluate Cell Migration

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Area of Science:

  • Gastroenterology
  • Cell Biology
  • Molecular Biology

Background:

  • Mucosal healing is a key therapeutic target for inflammatory bowel disease (IBD).
  • Rhamnogalacturonan (RGal) has previously demonstrated beneficial effects on intestinal epithelial barrier function.

Purpose of the Study:

  • To investigate the impact of RGal on intestinal epithelial wound healing.
  • To elucidate the molecular mechanisms underlying RGal-mediated wound repair.

Main Methods:

  • Utilized in vitro models including Caco-2, T84 cell lines, and primary colonoid monolayers subjected to wounding and RGal treatment.
  • Assessed cell proliferation and apoptosis using EdU and TUNEL assays, respectively.
  • Employed signaling pathway inhibitors and RNA sequencing (RNAseq) to identify involved pathways.
  • Evaluated RGal efficacy in a mouse model of DSS-induced colitis during the recovery phase.

Main Results:

  • RGal significantly enhanced wound healing in various intestinal cell models by increasing cell migration.
  • Inhibition of FAK, Src, PI3K, Rho family, and JNK signaling pathways reversed RGal's wound healing effects.
  • RNAseq analysis revealed upregulation of the NF-κB pathway following RGal treatment.
  • RGal treatment accelerated recovery from DSS-induced colitis in male mice, demonstrating in vivo efficacy.

Conclusions:

  • Rhamnogalacturonan (RGal) promotes intestinal epithelial wound healing through enhanced cell migration.
  • The mechanism involves pretranscriptional signaling pathways (FAK, Src, PI3K, Rho, JNK) and the NF-κB pathway.
  • RGal also accelerates mucosal healing in a preclinical model of colitis, suggesting therapeutic potential for IBD.