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.
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