Differential expression of sonic hedgehog immunoreactivity during lesion evolution in autoimmune encephalomyelitis.

Authors: Seifert, Thomas  Bauer, Jan  Weissert, Robert  Fazekas, Franz  Storch, Maria K 
Citation: Seifert T, etal., J Neuropathol Exp Neurol. 2005 May;64(5):404-11.
Pubmed: (View Article at PubMed) PMID:15892298

The signaling molecule Sonic hedgehog (Shh) is involved in several processes of central nervous system development. Recent reports indicate that Shh expression plays a role also in certain pathologic conditions in the adult brain, including multiple sclerosis and its animal model. However, the role of Shh signaling in immune-mediated demyelinating disease remains still uncertain. The aim of our study was to investigate the distribution pattern of Shh immunoreactivity (Shh-IR) during lesion evolution in myelin-oligodendrocyte-glycoprotein-induced experimental autoimmune encephalomyelitis (MOG-EAE), a model strongly mimicking multiple sclerosis. MOG-EAE was actively induced in DA rats. Histologic evaluation was performed with light and confocal microscopy on paraffin-embedded central nervous system sections from days 20 to 120 after active immunization. Shh-IR was present within the lesions of MOG-EAE during all stages of lesion evolution. The highest staining intensity for Shh was found in remyelinating lesions. In actively demyelinating, inactive demyelinated lesions, and in remyelinating lesions, Shh-IR was detected in macrophages, endothelium, and astrocytes. Shh-IR in axons was exclusively present in remyelinating lesions. Although the exact molecular mechanisms of the Shh-signaling pathway in experimental autoimmune encephalomyelitis are yet to be determined, our findings may imply a role of Shh signaling in facilitating remyelination.

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CRRD ID: 12801423
Created: 2017-03-29
Species: All species
Last Modified: 2017-03-29
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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.