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Metabolic Brain Disease

Erschienen in:

01.03.2012 | Original Paper

Contribution of GPR30 for 1,25 dihydroxyvitamin D₃ protection in EAE

verfasst von: Sandhya Subramanian, Lisa M. Miller, Marjorie R. Grafe, Arthur A. Vandenbark, Halina Offner

Erschienen in: Metabolic Brain Disease | Ausgabe 1/2012

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Abstract

Previous studies have demonstrated that vitamin D3-mediated protection in EAE occurs only in females and is dependent on the presence of diestrus levels of 17β-estradiol (E2). To evaluate the role of estrogen receptors in vitamin D3 treatment of EAE, we compared disease severity, CNS histopathology and immunological responses in vehicle and calcitrol (1,25 dihydroxyvitamin D₃) treated WT C57BL/6 mice vs. GPR30 membrane estrogen receptor (MER) knockout mice with MOG-35-55 peptide-induced EAE. Our results demonstrated that vitamin D₃-mediated prevention of clinical signs, CNS cellular lesions and demyelination observed in WT mice was abrogated in GPR30-KO mice with EAE. Regulatory effects of vitamin D₃ treatment that were MER dependent included increased levels of IL-10 and IL-6 secreted by MOG peptide-reactive splenocytes and increased expression of CCL5, CCR1 & CCR3 in spleen tissue. These results demonstrate for the first time that the MER is a key contributor to the E2-dependent effects of vitamin D₃-mediated protection in EAE.

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Titel: Contribution of GPR30 for 1,25 dihydroxyvitamin D3 protection in EAE
verfasst von: Sandhya Subramanian
Lisa M. Miller
Marjorie R. Grafe
Arthur A. Vandenbark
Halina Offner
Publikationsdatum: 01.03.2012
Verlag: Springer US
Erschienen in: Metabolic Brain Disease / Ausgabe 1/2012
Print ISSN: 0885-7490
Elektronische ISSN: 1573-7365
DOI: https://doi.org/10.1007/s11011-011-9266-6

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