| First Author | Becklund BR | Year | 2009 |
| Journal | Arch Biochem Biophys | Volume | 488 |
| Issue | 2 | Pages | 105-8 |
| PubMed ID | 19563774 | Mgi Jnum | J:154238 |
| Mgi Id | MGI:4367519 | Doi | 10.1016/j.abb.2009.06.015 |
| Citation | Becklund BR, et al. (2009) The calcitonin/calcitonin gene related peptide-alpha gene is not required for 1alpha,25-dihydroxyvitamin D3-mediated suppression of experimental autoimmune encephalomyelitis. Arch Biochem Biophys 488(2):105-8 |
| abstractText | The active form of vitamin D, 1alpha,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)), can suppress disease in the experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis. Calcium appears to be a critical component of 1,25(OH)(2)D(3)-mediated suppression of EAE, as complete disease prevention only occurs with a concomitant increase in serum calcium levels. Calcitonin (CT) is a peptide hormone released in response to acute increases in serum calcium, which led us to explore its importance in 1,25(OH)(2)D(3)-mediated suppression of EAE. Previously, we discovered that co-administration of pharmacological doses of CT enhanced the suppressive effect of 1,25(OH)(2)D(3) on EAE, suggesting CT may play a role in 1,25(OH)(2)D(3)-mediated suppression of EAE. To determine the importance of CT in EAE we have utilized a mouse strain in which the gene encoding CT and its alternative splice product, calcitonin gene related peptide-alpha (CGRP), have been deleted. Deletion of the CT/CGRP gene had no effect on EAE progression. Furthermore, treatment with 1,25(OH)(2)D(3) suppressed EAE in CT/CGRP knock-out mice equal to that in wild type mice. Therefore, we conclude that CT is not necessary for 1,25(OH)(2)D(3)-mediated suppression of EAE. |
