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Epithelial-derived fibronectin expression, signaling, and function in intestinal inflammation.

Vasantha L Kolachala1, Rahul Bajaj, Lixin Wang

  • 1Division of Digestive Diseases, Department of Medicine, Emory University, 615 Michael Street, Atlanta, GA 30322, USA.

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Fibronectin (FN) is abundant in the colon and its synthesis increases during colitis. This extracellular matrix protein promotes epithelial cell attachment and wound healing via integrin and NF-kappaB signaling.

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Area of Science:

  • Gastroenterology
  • Cell Biology
  • Molecular Biology

Background:

  • Fibronectin (FN) is a key extracellular matrix protein involved in cell functions.
  • The role and expression of FN in colitis, a condition of intestinal inflammation, remain largely unknown.
  • Understanding FN's function in the colon is crucial for addressing inflammatory bowel diseases.

Purpose of the Study:

  • To investigate the expression patterns of FN in the colon during intestinal inflammation.
  • To elucidate the regulatory mechanisms of FN synthesis in response to colitis.
  • To determine the functional role of FN in epithelial cell behavior during intestinal injury and healing.

Main Methods:

  • Utilized wild-type and transgenic mice models with dextran sodium sulfate (DSS)-induced colitis.
  • Employed immunohistochemistry and luciferase assays to quantify FN expression and promoter activity.
  • Conducted in vitro studies using the Caco2-BBE intestinal epithelial cell line.

Main Results:

  • Fibronectin (FN) is highly expressed by colonic surface epithelial cells in normal conditions.
  • FN synthesis was significantly upregulated during both the acute and healing phases of DSS-induced colitis.
  • In vitro, FN enhanced Caco2-BBE cell attachment and wound healing by upregulating alpha5beta1 integrin and activating NF-kappaB signaling, effects inhibited by RGD peptide and NF-kappaB inhibitors.

Conclusions:

  • Epithelial-derived fibronectin (FN) is abundantly synthesized by colonic cells and transcriptionally upregulated during colitis and recovery.
  • FN promotes epithelial cell attachment and wound healing through interactions with integrin receptors and activation of NF-kappaB signaling.
  • FN plays a critical role in maintaining epithelial integrity and regulating cellular responses to injury in the context of colitis.