Time dependency of 1,25(OH)2D3 induction of calbindin mRNA and calbindin expression in chick enterocytes during their differentiation along the crypt-villus axis

Parallel patterns of cell-specific gene expression during enterocyte differentiation and maturation in the small intestine of the rabbit

“…It is not always possible to state exactly the relationship between the pattern of mRNA accumulation as measured by in situ hybridisation and the transcription of a gene. In this instance however, the incorporation in RNA precursors into villus cells [44], and the rapid induction of calbindin expression by 1,25, (OH),D, in vitamin-D,-deficient chickens [49], suggest that the pattern of mRNA accumulation measured by this method here and in previous studies [16][17][18][19]491 may reflect a generalised pattern of transcriptional activity within these cells. The clear differences in the levels of each mRNA at a given point during a enterocyte differentiation and maturation are therefore likely to correspond to the level of transcription of that gene during its migration along the crypt-villus axis.…”

Transcriptional and translational control over sodium‐glucose‐linked transporter (SGLT1) gene expression in adult rat small intestine

“…Measurement of pre‐RNA levels and the ability of gene products to exhibit biological activities then gives further information about transcriptional and post‐translational processing. Gene expression can, however, also change in unpredictable ways during enterocyte migration along the crypt‐villus axis [5, 6]and this possibility should also be considered when describing any overall process of gene regulation in the small intestine [7].…”

Genomic analysis of 1,25-dihydroxyvitamin D3 action in mouse intestine reveals compartment and segment-specific gene regulatory effects

“…First, we did not evaluate 1,25(OH) 2 D 3 action on specific enterocyte lineages (e.g., absorptive epithelial cells versus secretory cells like goblet cells, Paneth cells, and enteroendocrine cells) nor did we examine any potential age-related effects on intestinal 1,25(OH) 2 D 3 action that might reflect ageassociated intestinal resistance to the hormone (63,64). Additionally, we used only one time for tissue harvest so we may have missed compartment-specific or gene-specific differences in 1,25(OH) 2 D 3 responsiveness, for example, similar to the induction of S100 g (calbindin D 9k ) by 1,25(OH) 2 D 3 that others reported was present in small intestinal villus but not in crypts (11). There is also a possibility that different cell extraction procedures required to isolate crypt epithelium versus duodenal epithelial compartments could lead to differences in measuring VDR binding between compartments-such potential differences should be considered when interpreting the data.…”

“…Several studies have shown that 1,25(OH) 2 D 3 action varies along the crypt–villus axis. In duodenal mid-villus cells, 1,25(OH) 2 D 3 rapidly stimulates calcium extrusion ( 10 ) but slower effects of 1,25(OH) 2 D 3 on crypt cells program the intestine for improved calcium absorption as the cells differentiate and migrate into the villus ( 11 ). Meanwhile, VDR loss increases colon epithelial cell proliferation and alters the contribution of Lgr5+ stem cells to the maintenance of the intestinal epithelium ( 12 , 13 ).…”