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Vitamin D deficiency enhances expression of autophagy-regulating miR-142-3p in mouse and 'involved' IBD patient intestinal tissues.

Vitamin D deficiency is an environmental factor involved in the pathogenesis of inflammatory bowel disease (IBD), however, the mechanisms surrounding its role remain unclear. Previous studies conducted in an intestinal epithelial-specific vitamin D receptor (VDR) knockout model suggest that a lack of vitamin D signaling causes a reduction in intestinal autophagy. A potential link between vitamin D deficiency and dysregulated autophagy is microRNA (miR)-142-3p, which suppresses autophagy. In this study, we found that wildtype C57BL/6 mice fed a vitamin D deficient diet for 5 weeks had increased miR-142-3p expression in ileal tissues compared to mice fed a matched control diet. Interestingly, there was no difference in expression of key autophagy markers ATG16L1 and LC3II in the ileum whole tissue. However, Paneth cells of vitamin D deficient mice were morphologically abnormal and had an accumulation of the autophagy adaptor protein p62 which was not present in the total crypt epithelium. These findings suggest that Paneth cells exhibit early markers of autophagy dysregulation within the intestinal epithelium in response to vitamin D deficiency and enhanced miR-142-3p expression. Finally, we demonstrated that treatment-naïve IBD patients with low levels of vitamin D have an increase in miR-142-3p expression in colonic tissues procured from 'involved' areas of disease. Taken together, our findings demonstrate that insufficient vitamin D levels alter expression of autophagy-regulating miR-142-3p in intestinal tissues of mice and IBD patients, providing insight into the mechanisms by which vitamin D deficiency modulates IBD pathogenesis.