scholarly journals Flow cytometry detection of vitamin D receptor changes during vitamin D treatment in Crohn's disease

2015 ◽  
Vol 181 (1) ◽  
pp. 19-28 ◽  
Author(s):  
M. Bendix ◽  
A. Dige ◽  
B. Deleuran ◽  
J. F. Dahlerup ◽  
S. P. Jørgensen ◽  
...  
2014 ◽  
Vol 8 ◽  
pp. S341
Author(s):  
O. Terjek ◽  
A.A. Csontos ◽  
K. Lorinczy ◽  
A. Bors ◽  
A. Torday ◽  
...  

2018 ◽  
Vol 24 (7) ◽  
pp. 1462-1470 ◽  
Author(s):  
Laura Gisbert-Ferrándiz ◽  
Pedro Salvador ◽  
Dolores Ortiz-Masiá ◽  
Dulce Carolina Macías-Ceja ◽  
Samuel Orden ◽  
...  

Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 973
Author(s):  
Laura Gisbert-Ferrándiz ◽  
Jesús Cosín-Roger ◽  
Carlos Hernández ◽  
Dulce C. Macias-Ceja ◽  
Dolores Ortiz-Masiá ◽  
...  

Vitamin D (VD) deficiency has been associated to Crohn’s disease (CD) pathogenesis, and the exogenous administration of VD improves the course of the disease, but the mechanistic basis of these observations remains unknown. Vitamin D receptor (VDR) mediates most of the biological functions of this hormone, and we aim to analyze here the expression of VDR in intestinal tissue, epithelial cells, and fibroblasts from CD patients. The effects of VD on a fibroblast wound healing assay and murine intestinal fibrosis are also analyzed. Our data show diminished VDR protein levels in surgical resections and epithelial cells from CD patients. In intestinal fibroblasts isolated from damaged tissue of CD patients, we detected enhanced migration and decreased VDR expression compared with both fibroblasts from non-damaged tissue of the same CD patient or control fibroblasts. Treatment with VD increased VDR protein levels, avoided the accelerated migration in CD fibroblasts, and prevented murine intestinal fibrosis induced by the heterotopic transplant model. In conclusion, our study demonstrates diminished VDR protein levels associated with enhanced migration in intestinal fibroblasts from damaged tissue of CD patients. In these cells, VD accumulates VDR and normalizes migration, which supports that CD patients would benefit from the VD anti-fibrotic therapeutic value that we demonstrate in a murine experimental model.


2015 ◽  
Vol 2015 ◽  
pp. 1-16 ◽  
Author(s):  
Marco Ardesia ◽  
Guido Ferlazzo ◽  
Walter Fries

Vitamin D deficiency has been recognized as an environmental risk factor for Crohn’s disease since the early 80s. Initially, this finding was correlated with metabolic bone disease. Low serum 25-hydroxyvitamin D levels have been repeatedly reported in inflammatory bowel diseases together with a relationship between vitamin D status and disease activity. Subsequently, low serum vitamin D levels have been reported in various immune-related diseases pointing to an immunoregulatory role. Indeed, vitamin D and its receptor (VDR) are known to interact with different players of the immune homeostasis by controlling cell proliferation, antigen receptor signalling, and intestinal barrier function. Moreover, 1,25-dihydroxyvitamin D is implicated in NOD2-mediated expression of defensin-β2, the latter known to play a crucial role in the pathogenesis of Crohn’s disease (IBD1 gene), and several genetic variants of the vitamin D receptor have been identified as Crohn’s disease candidate susceptibility genes. From animal models we have learned that deletion of the VDR gene was associated with a more severe disease. There is a growing body of evidence concerning the therapeutic role of vitamin D/synthetic vitamin D receptor agonists in clinical and experimental models of inflammatory bowel disease far beyond the role of calcium homeostasis and bone metabolism.


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