TGF-β1 and TGF-β2 expression after traumatic human spinal cord injury

被引：70

作者：

Buss, A. ^{[1
]}

Pech, K. ^{[1
]}

Kakulas, B. A. ^{[2
]}

Martin, D. ^{[3
]}

Schoenen, J. ^{[4
,5
]}

Noth, J. ^{[1
]}

Brook, G. A. ^{[1
,6
]}

机构：

[1] Rhein Westfal TH Aachen, Dept Neurol, Aachen Univ Hosp, D-52074 Aachen, Germany

[2] Univ Western Australia, Ctr Neuromuscular & Neurol Disorders, Perth, WA 6009, Australia

[3] Univ Liege, Dept Neurosurg, Sart Tilman Hosp, Liege, Belgium

[4] Univ Liege, Dept Neurol, Liege, Belgium

[5] Univ Liege, Dept Neuroanat, Liege, Belgium

[6] Rhein Westfal TH Aachen, Dept Neuropathol, Aachen Univ Hosp, D-52074 Aachen, Germany

来源：

SPINAL CORD | 2008年 / 46卷 / 05期

关键词：

spinal cord injury; Wallerian degeneration; scar; inflammation;

D O I：

10.1038/sj.sc.3102148

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Study design: Immunohistochemical investigation in control and lesioned human spinal cords. Objectives: To assess the spatial and temporal expression patterns of transforming growth factor-beta 1 and -beta 2 (TGF-beta 1 and TGF-beta 2) in the human spinal cord after traumatic injury. Setting: Germany, Aachen, Aachen University Hospital. Methods: Sections from human spinal cords from 4 control patients and from 14 patients who died at different time points after traumatic spinal cord injury (SCI) were investigated immunohistochemically. Results: In control cases, TGF-beta 1 was confined to occasional blood vessels, intravascular monocytes and some motoneurons, whereas TGF-beta 2 was only found in intravascular monocytes. After traumatic SCI, TGF-beta 1 immunoreactivity was dramatically upregulated by 2 days after injury (the earliest survival time investigated) and was detected within neurons, astrocytes and invading macrophages. The staining was most intense over the first weeks after injury but gradually declined by 1 year. TGF-beta 2 immunoreactivity was first detected 24 days after injury. It was located in macrophages and astrocytes and remained elevated for up to 1 year. In white matter tracts undergoing Wallerian degeneration, there was no induction of either isoform. Conclusion: The early induction of TGF-beta 1 at the point of SCI suggests a role in the acute inflammatory response and formation of the glial scar, while the later induction of TGF-beta 2 may indicate a role in the maintenance of the scar. Neither of these TGF-beta isoforms appears to contribute to the astrocytic scar formation in nerve fibre tracts undergoing Wallerian degeneration.

引用

页码：364 / 371

页数：8

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