TGF-β1 and TGF-β2 expression after traumatic human spinal cord injury
TGF-β1 and TGF-β2 expression after traumatic human spinal cord injury
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DOI：
10.1038/sj.sc.3102148
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发表时间：
2008-05-01
期刊：
影响因子：
2.2
通讯作者：
Brook, G. A.
中科院分区：
文献类型：
--
作者：
Buss, A.;Pech, K.;Brook, G. A.
研究设计：对照和损伤人脊髓的免疫组织化学研究。目的：研究转化生长因子-β1和转化生长因子-β2在创伤后人脊髓中的时空表达模式。地点：德国亚琛亚琛大学医院。方法：对4例对照组和14例创伤性脊髓损伤后不同时间死亡的患者的脊髓切片进行免疫组织化学研究。结果：在对照组中，转化生长因子-β1仅局限于偶见的血管、血管内单核细胞和部分运动神经元，而转化生长因子-β2仅见于血管内单核细胞。创伤性脊髓损伤后2d(最早存活时间)，转化生长因子-β1免疫反应显著上调，在神经元、星形胶质细胞和侵袭性巨噬细胞中均可检测到。在损伤后的头几周，染色最强烈，但在一年后逐渐减弱。在伤后24天首次检测到转化生长因子-β2免疫反应。它位于巨噬细胞和星形胶质细胞中，并持续升高长达一年。结论：早期在脊髓损伤时诱导的转化生长因子-β1可能参与了急性炎症反应和胶质瘢痕的形成，而后期的转化生长因子-β2的诱导可能在瘢痕的维持中起作用。这两种转化生长因子-β亚型似乎都不是沃勒变性神经纤维束中星形细胞瘢痕形成的原因。
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.