scholarly journals MiR-125a-5p Regulates Vitamin D Receptor Expression in a Mouse Model of Experimental Autoimmune Encephalomyelitis

2019 ◽  
Vol 36 (2) ◽  
pp. 110-120 ◽  
Author(s):  
Han-Chun Long ◽  
Rui Wu ◽  
Chun-Feng Liu ◽  
Fei-Long Xiong ◽  
Zu Xu ◽  
...  
Keyword(s):  
Vitamin D ◽  
Mouse Model ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Vitamin D Receptor ◽  
Receptor Expression ◽  
Autoimmune Encephalomyelitis ◽  
Experimental Autoimmune

scholarly journals UV light suppression of EAE (a mouse model of multiple sclerosis) is independent of vitamin D and its receptor

2019 ◽  
Vol 116 (45) ◽  
pp. 22552-22555 ◽  
Author(s):  
Amy A. Irving ◽  
Steven J. Marling ◽  
Jeremy Seeman ◽  
Lori A. Plum ◽  
Hector F. DeLuca
Keyword(s):  
Multiple Sclerosis ◽  
Vitamin D ◽  
Mouse Model ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Uv Light ◽  
Protective Action ◽  
Ultra Violet ◽  
Uv Exposure ◽  
Autoimmune Encephalomyelitis ◽  
Experimental Autoimmune

Vitamin D and sunlight have each been reported to protect against the development of experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis (MS). To date, the contribution of each has been unclear as ultra violet (UV) exposure also causes the generation of vitamin D in the skin. To examine whether the UV based suppression of EAE results, at least, in part from the production of vitamin D, we studied the effect of UV light on EAE in mice unable to produce 7-dehydroxycholesterol (7-DHC), the required precursor of vitamin D. Furthermore, we examined UV suppression of EAE in mice devoid of the vitamin D receptor (VDR). Our results demonstrate that UV light suppression of EAE occurs in the absence of vitamin D production and in the absence of VDR. Future investigations will focus on identifying the pathway responsible for the protective action of UV in EAE and presumably human MS.

scholarly journals A Nonsecosteroidal Vitamin D Receptor Modulator Ameliorates Experimental Autoimmune Encephalomyelitis without Causing Hypercalcemia

2011 ◽  
Vol 2011 ◽  
pp. 1-14 ◽  
Author(s):  
Songqing Na ◽  
Yanfei Ma ◽  
Jingyong Zhao ◽  
Clint Schmidt ◽  
Qing Q. Zeng ◽  
...  
Keyword(s):  
Vitamin D ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Vitamin D Receptor ◽  
Type I Diabetes ◽  
Biologically Active ◽  
Type I ◽  
Autoimmune Encephalomyelitis ◽  
Compound A ◽  
Cytokine Analysis ◽  
Experimental Autoimmune

Vitamin D receptor (VDR) agonists are currently the agents of choice for the treatment of psoriasis, a skin inflammatory indication that is believed to involve an autoimmune component. 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3], the biologically active metabolite of vitamin D, has shown efficacy in animal autoimmune disease models of multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease, and type I diabetes. However, the side effect of 1,25-(OH)2D3and its synthetic secosteroidal analogs is hypercalcemia, which is a major impediment in their clinical development for autoimmune diseases. Hypercalcemia develops as a result of the action of VDR agonists on the intestine. Here, we describe the identification of a VDR modulator (VDRM) compound A that was transcriptionally less active in intestinal cells and as a result exhibited less calcemic activityin vivothan 1,25-(OH)2D3. Cytokine analysis indicated that the VDRM not only modulated the T-helper cell balance from Th1 to Th2 effector function but also inhibited Th17 differentiation. Finally, we demonstrate that the oral administration of compound A inhibited the induction and progress of experimental autoimmune encephalomyelitis in mice without causing hypercalcemia.

Vitamin D down-regulates the expression of some Th17 cell-related cytokines, key inflammatory chemokines, and chemokine receptors in experimental autoimmune encephalomyelitis

2018 ◽  
Vol 22 (10) ◽  
pp. 725-737 ◽  
Author(s):  
Abdollah Jafarzadeh ◽  
Sayyed Vahab Azizi ◽  
Zahra Arabi ◽  
Rayhaneh Ahangar-Parvin ◽  
Marziyeh Mohammadi-Kordkhayli ◽  
...  
Keyword(s):  
Vitamin D ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Chemokine Receptors ◽  
Th17 Cell ◽  
Autoimmune Encephalomyelitis ◽  
Inflammatory Chemokines ◽  
Experimental Autoimmune
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