脊髓损伤会诱导促炎和抗血管生成细胞因子EMAP II在损伤部位表达。

Spinal cord injury induces lesional expression of the proinflammatory and antiangiogenic cytokine EMAP II.

作者信息

Mueller Christian-Andreas, Schluesener Hermann J, Conrad Sabine, Meyermann Richard, Schwab Jan M

机构信息

Institute of Brain Research, Eberhard-Karls University Tuebingen, Tuebingen, Germany.

出版信息

J Neurotrauma. 2003 Oct;20(10):1007-15. doi: 10.1089/089771503770195858.

DOI:10.1089/089771503770195858

PMID:14588117

Abstract

Inflammatory cellular responses to spinal cord injury are promoted by proinflammatory messengers. We have analyzed expression of endothelial monocyte activating polypeptide II (EMAP II), a proinflammatory, antiangiogenic cytokine in rats after spinal cord injury (SCI) in comparison to normal rat spinal cords. Immunohistochemical analysis demonstrated a highly significant (p < 0.0001) accumulation of EMAP II(+) microglia/macrophages at the lesion site compared to remote areas and uninjured controls. After peaking at day 3, EMAP II(+) microglia/macrophage cell numbers declined gradually until day 28 after SCI-but still remained elevated. Further, EMAP II(+) cells formed clusters in perivascular Virchow-Robin spaces reaching a maximum at day 3. Prolonged accumulation of EMAP II(+), ED1(+) microglia/macrophages suggest a role of EMAP II in the pathophysiology of secondary injury following SCI.

摘要

促炎信使可促进对脊髓损伤的炎症细胞反应。我们分析了与正常大鼠脊髓相比，脊髓损伤（SCI）后大鼠体内促炎、抗血管生成细胞因子内皮单核细胞激活多肽II（EMAP II）的表达。免疫组织化学分析表明，与远处区域和未受伤对照相比，损伤部位EMAP II(+)小胶质细胞/巨噬细胞有高度显著（p < 0.0001）的积聚。在第3天达到峰值后，EMAP II(+)小胶质细胞/巨噬细胞数量逐渐下降，直到SCI后第28天——但仍保持升高。此外，EMAP II(+)细胞在血管周围的Virchow-Robin间隙形成簇，在第3天达到最大值EMAP II(+)、ED1(+)小胶质细胞/巨噬细胞的长期积聚表明EMAP II在SCI后继发性损伤的病理生理学中起作用。