Diminished Vitamin D Receptor Protein Levels in Crohn’s Disease Fibroblasts: Effects of Vitamin D
Nutrients 2020, 12(4), 973; https://doi.org/10.3390/nu12040973
Laura Gisbert-Ferrándiz 1,†OrcID,Jesús Cosín-Roger 2,†,Carlos Hernández 2OrcID,Dulce C. Macias-Ceja 2,Dolores Ortiz-Masiá 3,Pedro Salvador 1,Juan V. Esplugues 1,2OrcID,Joaquín Hinojosa 4,Francisco Navarro 4OrcID,Sara Calatayud 1OrcID andMaría D. Barrachina 1,*
Items in both categories Gut and Vitamin D Receptor are listed here:
- Crohn’s Disease is associated with poor Vitamin D Receptor (many solutions) – April 2020
- Microbiomes of both gut and airway are affected by Vitamin D and Vitamin D Receptor – Nov 2018
- Vitamin D Receptor, the gut, the immune system, and the Middle East – May 2019
- Inflammatory bowel disease, gut bionome and Vitamin D Receptor – 2018
- Resveratrol Role in Autoimmune Disease-A Mini-Review. – Dec 2016
- Immunological effects of vitamin D and their relations to autoimmunity – March 2019
- Gut and airway bionome are affected by Vitamin D and Vitamin D Receptor – Nov 2018
- Inflammation and immune responses to Vitamin D (perhaps need to measure active vitamin D) – July 2017
- Ulcerative Colitis – half have poor level of Vitamin D Receptor vs only one in ten normally – June 2017
- Ulcerative colitis associated with both low Vitamin D and poor Vitamin D Receptors – Oct 2016
- Crohn's disease associated with 7.6X deactivation of Vitamin D receptor – July 2015
Vitamin D Receptor is associated in over 58 autoimmune studies
The risk of 44 diseases at least double with poor Vitamin D Receptor as of Oct 2019
Vitamin D Receptor activation can be increased by any of: Resveratrol, Omega-3, Magnesium, Zinc, Quercetin, non-daily Vit D, Curcumin, intense exercise, Ginger, Essential oils, etc Note: The founder of Vitamin D Life uses 10 of the 12 known VDR activators
Resveratrol improves health (Vitamin D receptor, etc.) has the following
- The Vitamin D Receptor can restrict how much of the Vitamin D in the blood actually gets to cells
- Resveratrol is one of 11 ways to negate the Vitamin D Receptor restrictions
- Resveratrol is produced by several plants in response to injury or, when the plant is under attack by pathogens such as bacteria or fung
- Benefits of Reseveratrol, like Vitamin D, appears to be increased when used with other things
- Quercetin and Curcumin in the case of Resveratro
The articles in both of the categories Resveratrol and Vitamin D Receptor
- Vitamin D Receptor activation should reduce ARDS associated with CVOID-19 - June 2020
- Cognitive decline not helped by daily vitamin D getting to just 30 ng – RCT July 2019
- Resveratrol prevented bone loss associated with T2DM (probably via VDR) – RCT Sept 2018
- Effects of Resveratrol against Lung Cancer in mice – Nov 2017
- Resveratrol Role in Autoimmune Disease-A Mini-Review. – Dec 2016
- Lifespan and healthspan extension by resveratrol - Jan 2015
- Resveratrol and Cardiovascular Diseases – May 2016
- Resveratrol improves health (Vitamin D receptor, etc.)
- Bone density improved with resveratrol (which improves Vitamin D Receptor) – RCT Sept 2018
- Natural Ways to Increase Calcitriol and Activate The Vitamin D Receptor Gene – Oct 2017
- Immune system is aided by red grapes, blueberries, both of which increase Vitamin D receptor – 2013
- Resveratol helps vitamin D bind to cells – Dec 2014
- Resveratrol gets vitamin D to cells even if poor vitamin D receptor
Download the PDF from Vitamin D Life
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