OBJECTIVE: Cerebral ischemia triggers acute inflammation, which exacerbates primary brain damage. Characterization of cytokine expression to the early damaged tissue might aid in further understanding of lesion development and contribute to definition of molecular targets for selective immunotherapy. Endothelial monocyte-activating polypeptide II (EMAPII) is a proinflammatory, antiangiogenic cytokine whose expression following cerebral ischemia remained unknown. Therefore, we studied the spatiotemporal expression of EMAPII in early brain lesions after cerebral ischemia-reperfusion injury. METHODS: Unilateral transient focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) for 1 hr followed by different reperfusion periods using male Sprague-Dawley rats. Subsequently, rats were sacrificed on Day 1, 3, 5, or 7 following surgery. EMAPII expression was investigated by immunohistochemistry. RESULTS: EMAPII-positive cell accumulation was observed as early as Day 1 postreperfusion and increased steadily. Significant accumulation of EMAPII-positive cells was seen in lesion and penumbra areas but not in the translateral hemisphere. Both amoeboid and ramified EMAPII-positive cells were observed and mainly localized to lesion and penumbra areas, respectively. CONCLUSION: The known pathological functions together with abundant cellular accumulation in cerebral ischemia lesions suggest that EMAPII might contribute to pathophysiological consequences of cerebral ischemia.
OBJECTIVE:Cerebral ischemia triggers acute inflammation, which exacerbates primary brain damage. Characterization of cytokine expression to the early damaged tissue might aid in further understanding of lesion development and contribute to definition of molecular targets for selective immunotherapy. Endothelial monocyte-activating polypeptide II (EMAPII) is a proinflammatory, antiangiogenic cytokine whose expression following cerebral ischemia remained unknown. Therefore, we studied the spatiotemporal expression of EMAPII in early brain lesions after cerebral ischemia-reperfusion injury. METHODS: Unilateral transient focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) for 1 hr followed by different reperfusion periods using male Sprague-Dawley rats. Subsequently, rats were sacrificed on Day 1, 3, 5, or 7 following surgery. EMAPII expression was investigated by immunohistochemistry. RESULTS: EMAPII-positive cell accumulation was observed as early as Day 1 postreperfusion and increased steadily. Significant accumulation of EMAPII-positive cells was seen in lesion and penumbra areas but not in the translateral hemisphere. Both amoeboid and ramified EMAPII-positive cells were observed and mainly localized to lesion and penumbra areas, respectively. CONCLUSION: The known pathological functions together with abundant cellular accumulation in cerebral ischemia lesions suggest that EMAPII might contribute to pathophysiological consequences of cerebral ischemia.