The Calcitonin / Calcitonin Gene Related Peptide-alpha Gene is not Required for 1alpha,25-Dihyrdroxyvitamin D(3)-mediated Suppression of Experimental Autoimmune Encephalomyelitis. Archives of biochemistry and biophysics [Arch Biochem Biophys] Journal article | | Title | The Calcitonin / Calcitonin Gene Related Peptide-alpha Gene is not Required for 1alpha,25-Dihyrdroxyvitamin D(3)-mediated Suppression of Experimental Autoimmune Encephalomyelitis. | | Author(s) | Becklund BR, James BJ, Gagel RF, Deluca HF | | Institution | Department of Biochemistry, University of Wisconsin-Madison, Madison, WI. | | Source | Arch Biochem Biophys 2009 Jun 26. | | Abstract | 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. | | Language | ENG | | Pub Type(s) | JOURNAL ARTICLE
| | PubMed ID | 19563774 |
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