Immunohistochemical studies on disabled-2 protein in the spinal cords of rats with experimental autoimmune encephalomyelitis.

Authors: Ahn, M  Oh, H  Lee, W  Kim, H  Moon, C  Shin, T 
Citation: Ahn M, etal., Brain Res. 2011 Oct 6;1416:51-60. doi: 10.1016/j.brainres.2011.08.009. Epub 2011 Aug 10.
Pubmed: (View Article at PubMed) PMID:21890121
DOI: Full-text: DOI:10.1016/j.brainres.2011.08.009

Disabled-2 (Dab-2), an adaptor protein of transforming growth factor beta (TGF-beta) signaling, was studied in the spinal cords of rats with experimental autoimmune encephalomyelitis (EAE) to evaluate the possible involvement of Dab-2 in the pathogenesis of EAE using Western blot and immunohistochemical analyses. Western blot analysis showed that two isoforms (p96 kDa and p67 kDa) of Dab-2 were detected in the spinal cords of rats used as controls. Both isoforms of Dab-2 were significantly elevated in the EAE spinal cord at the peak stage of EAE (P<0.05) and declined at the recovery stage. However, only the p96 kDa isoform was markedly phosphorylated in the EAE spinal cord. Immunohistochemistry showed that Dab-2 and p-Dab-2 were detected in some vascular endothelial cells, glial cells, and some neurons in the rat spinal cords of normal and immunized CFA-alone controls. In EAE lesions, Dab-2 and p-Dab-2 were immunodetected in some inflammatory cells (mainly in ED1-positive macrophages and R73-positive T cells), while the enhanced immunoreactivity of Dab-2 in spinal cord cells suggested constitutive expression. Additionally, TGF-beta1 immunoreactivity showed a similar expression pattern of Dab-2 in EAE lesions. These findings suggest that Dab-2 is transiently upregulated and phosphorylated (particularly the p96 kDa isoform) in EAE, a CNS autoimmune disease, and may be involved in TGF-beta signaling.

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CRRD ID: 7243155
Created: 2013-05-09
Species: All species
Last Modified: 2013-05-09
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.