Lesional expression of the endogenous angiogenesis inhibitor endostatin/collagen XVIII following traumatic brain injury (TBI)

被引：22

作者：

Mueller, C. A. ^{[1
,2
]}

Schluesener, H. J. ^{[2
]}

Fauser, U. ^{[2
]}

Conrad, S. ^{[2
,3
]}

Schwab, J. M. ^{[2
,4
]}

机构：

[1] Univ Bonn, Dept Neurosurg, D-53105 Bonn, Germany

[2] Univ Tubingen, Sch Med, Inst Brain Res, D-72076 Tubingen, Germany

[3] Univ Tubingen, Sch Med, Div Tissue Engn, Inst Anat, Tubingen, Germany

[4] Humboldt Univ, Charite Med Sch, Dept Neurol & Experimental Neurol, D-10117 Berlin, Germany

来源：

EXPERIMENTAL NEUROLOGY | 2007年 / 208卷 / 02期

关键词：

CNS injury; vascular remodelling; antiangiogenesis;

D O I：

10.1016/j.expneurol.2007.07.020

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

We have analysed the expression of the endogenous angiogenesis inhibitor endostatin/collagen XVIII following stab wound injury and observed a highly significant (p < 0.0001) lesional accumulation confined to areas of pan-necrotic injury and developing secondary damage. Maximal cell numbers were detected at Day 14, declining until Day 21 after injury. Further, endostatin/collagen XVIII+ monocytic cells accumulated in Virchow-Robin spaces where they formed cell clusters. Besides being prevailingly localised to ED1(+) activated microglia/macrophages, endostatin/collagen XVIII expression was also detected by subendothelial surrounding vessels in the lesioned area. Late and prolonged accumulation of endostatin/collagen XVIII+ microglia/macrophages and increased numbers of endostatin/collagen XVIII+ subendothelial cells/vessels in areas of vascular pruning and regression, point to a role in the termination of the transient angiogenic response, linked to a "late" inflammatory milieu. (c) 2007 Elsevier Inc. All rights reserved.

引用

页码：228 / 237

页数：10

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