The following is a summary of “Influence of vitamin D receptor signaling and vitamin D on colonic epithelial cell fate decisions in ulcerative colitis,” published in the May 2024 issue of Gastroenterology by Kellermann et al.
Existing evidence suggests a link between low vitamin D (25(OH)D) levels and a more severe form of ulcerative colitis (UC). In contrast, a growing interest in understanding how vitamin D receptor (VDR) signaling might influence UC.
Researchers conducted a retrospective study to examine the effects of active vitamin D (1,25(OH)2D3) and VDR signaling on the health of human colon epithelial cells grown in organoids.
They examined intestinal VDR expression through immunohistochemistry, RNA expression arrays, and single-cell RNA sequencing of colonic biopsy specimens from patients with UC and healthy controls. Patient-derived colonic organoids were utilized to understand the functional and transcriptional impacts of 1,25(OH)2D. The role of VDR dependency was evaluated by employing CRISPR/Cas9 to knock out the receptor.
The results showed that 1,25(OH)2D3/VDR stimulation facilitates colonic epithelium differentiation. Impaired 1,25(OH)2D3/VDR signaling may compromise the integrity of the intestinal epithelial barrier, potentially exacerbating UC flares. Additionally, transcriptional response to VDR activity was primarily observed in fully differentiated cells at the apex of the colonic crypt, with this response diminishing during UC flares.
Investigators concluded that exposure to active vitamin D (1,25(OH)2D3) and human colonic organoids in VDR signaling supported epithelial cell health.
Source: academic.oup.com/ecco-jcc/advance-article/doi/10.1093/ecco-jcc/jjae074/7673983