Spinal cord injury induces differential expression of the profibrotic semaphorin 7A in the developing and mature glial scar.

Abstract:

:Semaphorin 7A (Sema7A) is involved in the formation of the central nervous system during development by operating axon guidance and neuronal migration. We investigated the expression of the TGFβ-inducible Sema7A following spinal cord injury (SCI). After SCI, Sema7A(+) cells accumulated specifically in lesion areas resulting in significantly enhanced Sema7A expression at the injury site (P < 0.0001). During the first days lesional Sema7A expression was confined to neurons, ballooned neurite fibers/retraction bulbs, and endothelial cells. At day 7, we observed Sema7A expression by components of the glial scar, such as reactive astrocytes and pronounced extracellular Sema7A deposition. In the direct perilesional rim, Sema7A(+) astrocytes coexpressed the activation-associated intermediate filament vimentin. In the injured spinal cord, numbers of Sema7A(+) cells reached maximum levels at day 14. The restricted accumulation of Sema7A(+) reactive astrocytes and Sema7A deposition in fibronectin(+) extracellular matrix territories suggests a participation of the fibrostimulatory Sema7A in the developing and maturating scar following SCI. In addition, Sema7A appears to be marker a for astrocyte activation.

journal_name

Glia

journal_title

Glia

authors

Kopp MA,Brommer B,Gatzemeier N,Schwab JM,Prüss H

doi

10.1002/glia.21045

subject

Has Abstract

pub_date

2010-11-01 00:00:00

pages

1748-56

issue

14

eissn

0894-1491

issn

1098-1136

journal_volume

58

pub_type

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