Collagen Boosts Cell Regeneration in Gut Injury

According to a new study published in Inflammation and Regeneration, researchers from Tokyo Medical and Dental University (TMDU) have identified a physical cue that stimulates cells in the human gut to go from old to young again. The TMDU study found that collagen deposition at sites of intestinal injury promotes the conversion of mature intestinal cells into fetal-like cells that can generate new healthy tissue to repair the injury.

The process of converting mature intestinal cells into fetal-like cells is known to occur during the inflammatory response that often follows tissue injury. This process of regenerating injured tissues is important for repairing damaged areas of the intestine. To better understand the mechanisms behind this process, the TMDU researchers created collagen spheres from both mouse and human intestinal cells and assessed gene expression in these spheres.

The results of the study revealed that culturing in collagen induced the expression of inflammation-associated and fetal-like genes in both types of cells. These findings suggest that collagen has a significant influence on inflammation and cellular reprogramming in both mice and humans.

Importantly, the representative genes activated in the human collagen spheres were also highly expressed in tissue samples taken from inflamed gut regions in patients with ulcerative colitis. This suggests that these findings may have implications for understanding the role of inflammation in conditions such as colorectal cancer.

The TMDU researchers also found that the YAP/TAZ-TEAD axis plays a central role in the induction of the distinctive gene expression signature associated with converting mature intestinal cells into fetal-like cells. In addition, they identified the cooperative transcriptional activity of Fra1 and RUNX2 in this process, which plays a role in the gene network centered on fibronectin.

This study’s findings demonstrate that collagen significantly influences inflammation and cellular reprogramming in both mice and humans. Further research using this model may help to enhance our understanding of how the extracellular environment influences inflammation and how other disease processes occur in the gut.