Journal
MULTIPLE SCLEROSIS JOURNAL
Volume 21, Issue 13, Pages 1632-1643Publisher
SAGE PUBLICATIONS LTD
DOI: 10.1177/1352458515599848
Keywords
Semaphorin; multiple sclerosis; demyelination; neurodegeneration; neuroregeneration and neuroinflammation
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Funding
- FIS of the Ministry of Economy and Competitiveness of Spain [PI12/02144]
- PFIS programme through the FIS of the Ministry of Economy and Competitiveness of Spain [FI10/00456]
- 'Sara Borrell' programme through the FIS of the Ministry of Economy and Competitiveness of Spain [CD09/00363]
- 'Miguel Servet' programme through the FIS of the Ministry of Economy and Competitiveness of Spain [CP07/00146, CP13/00028]
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Background: Studies in multiple sclerosis (MS) and in experimental models point to a critical role of semaphorin (sema)3A and sema7A in MS pathogenesis. Objective: The objective of this paper is to characterise the expression of sema3A, sema7A, and their receptors in MS lesions. Methods: We included 44 demyelinating lesions from MS patients, 12 lesions with acute cerebral infarct, 11 lesions with progressive multifocal leucoencephalopathy and 10 non-neurological control patients. MS lesions were classified according to inflammatory activity and all samples were immunostained for sema3A, sema7A, neuropilin 1 (Np-1), 1-integrin, and 1-integrin. Results: In MS-damaged white matter sema3A and Np-1 were both detected in microglia/macrophages, whereas reactive astrocytes expressed only sema3A. Otherwise, sema7A, 1-integrin and 1-integrin were observed in reactive astrocytes, and microglia/macrophages only expressed 1-integrin. The expression of sema3A, sema7A and their receptors is more relevant in MS than in other demyelinating diseases. Sema3A and sema7A expression correlated with the inflammatory activity of the MS lesions, suggesting their involvement in the immunological process that takes place in MS. Conclusions: The expression pattern of sema3A, sema7A and their receptors in MS lesions suggests that both molecules contribute to create a negative environment for tissue regeneration, influencing the ability to regenerate the damaged tissue.
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