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Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice
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Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice

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HucMSC-Ex alleviates inflammatory bowel disease by regulating O-GlcNAcylation modification of RACK1 in intestinal

Ziyue Liu1, Jintao Yuan2, Muhammad AzharUd Din1

  • 1Department of Laboratory Medicine, the Affiliated People's Hospital, Jiangsu University, Zhenjiang, Jiangsu 212002, PR China.

Colloids and Surfaces. B, Biointerfaces
|March 11, 2025
PubMed

Inflammatory Bowel Disease (IBD) is a chronic autoimmune disorder that severely affects the gastrointestinal tract and is difficult to cure. This study explored the mechanism by which human umbilical cord mesenchymal stem cell-derived exosomes (HucMSC-Ex) alleviate IBD through O-GlcNAc glycosylation modification and the expression of related proteins. The study analyzed the effects of HucMSC-Ex on the inhibition of pro-inflammatory factors and promotion of intestinal epithelial cells regeneration in vitro and in vivo, with a focus on the role of the O-GlcNAc glycosylation of the RACK1 protein. The findings indicated that HucMSC-Ex reverses epithelial-mesenchymal transition (EMT) by upregulating O-GlcNAc glycosylation levels and effectively alleviates IBD symptoms and inflammatory responses in mouse intestinal epithelial cells. By modulating O-GlcNAc glycosylation, HucMSC-Ex exhibits significant therapeutic potential in immune regulation and gut microbiota remodeling, offering new perspectives for IBD treatment.

Keywords:
EMTHucMSC-ExIBDO-GlcNAcRACK1

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