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It has been hypothesized that apically expressed L-type Ca 2+ channel Ca v 1.3 (encoded by CACNA1D gene) contributes toward an alternative TRPV6-independent route of intestinal epithelial Ca 2+ absorption, especially during digestion when high luminal concentration of Ca 2+ and other nutrients limit TRPV6 contribution. We and others have implicated altered expression and activity of key mediators of intestinal and renal Ca 2+ (re)absorption as contributors to negative systemic Ca 2+ balance and bone loss in intestinal inflammation. Here, we investigated the effects of experimental colitis and related inflammatory mediators on colonic Ca v 1.3 expression. We confirmed Ca v 1.3 expression within the segments of the mouse and human gastrointestinal tract. Consistent with available microarray data (GEO database) from inflammatory bowel disease (IBD) patients, mouse colonic expression of Ca v 1.3 was significantly reduced in trinitrobenzene sulfonic acid (TNBS) colitis. In vitro, IFNγ most potently reduced Ca v 1.3 expression. We reproduced these findings in vivo with wild-type and Stat1 −/− mice injected with IFNγ. The observed effect in Stat1 −/− suggested a noncanonical transcriptional repression or a posttranscriptional mechanism. In support of the latter, we observed no effect on the cloned Ca v 1.3 gene promoter activity and accelerated Ca v 1.3 mRNA decay rate in IFNγ-treated HCT116 cells. While the relative contribution of Ca v 1.3 to intestinal Ca 2+ absorption and its value as a therapeutic target remain to be established, we postulate that Ca v 1.3 downregulation in IBD may contribute to the negative systemic Ca 2+ balance, to increased bone resorption, and to reduced bone mineral density in IBD patients.

Expression of Cav1.3 calcium channel in the human and mouse colon: posttranscriptional inhibition by IFNγ

Expression of Ca_v1.3 calcium channel in the human and mouse colon: posttranscriptional inhibition by IFNγ