Induction of secretory phospholipase A2 in reactive astrocytes in response to transient focal cerebral ischemia in the rat brain
Journal of neurochemistry, 2004•Wiley Online Library
Although mRNA expression of group IIA secretory phospholipase A2 (sPLA2‐IIA) has been
implicated in responses to injury in the CNS, information on protein expression remains
unclear. In this study, we investigated temporal and spatial expression of sPLA2‐IIA mRNA
and immunoreactivity in transient focal cerebral ischemia induced in rats by occlusion of the
middle cerebral artery. Northern blot analysis showed a biphasic increase in sPLA2‐IIA
mRNA expression following 60‐min of ischemia–reperfusion: an early phase at 30 min and …
implicated in responses to injury in the CNS, information on protein expression remains
unclear. In this study, we investigated temporal and spatial expression of sPLA2‐IIA mRNA
and immunoreactivity in transient focal cerebral ischemia induced in rats by occlusion of the
middle cerebral artery. Northern blot analysis showed a biphasic increase in sPLA2‐IIA
mRNA expression following 60‐min of ischemia–reperfusion: an early phase at 30 min and …
Abstract
Although mRNA expression of group IIA secretory phospholipase A2 (sPLA2‐IIA) has been implicated in responses to injury in the CNS, information on protein expression remains unclear. In this study, we investigated temporal and spatial expression of sPLA2‐IIA mRNA and immunoreactivity in transient focal cerebral ischemia induced in rats by occlusion of the middle cerebral artery. Northern blot analysis showed a biphasic increase in sPLA2‐IIA mRNA expression following 60‐min of ischemia–reperfusion: an early phase at 30 min and a second increase at a late phase ranging from 12 h to 14 days. In situ hybridization localized the early‐phase increase in sPLA2‐IIA mRNA to the affected ischemic cortex and the late‐phase increase to the penumbral area. Besides sPLA2‐IIA mRNA, glial fibrillary acidic protein (GFAP) and cyclo‐oxygenase‐2 mRNAs, but not cytosolic PLA2, also showed an increase in the penumbral area at 3 days after ischemia–reperfusion. Immunohistochemistry of sPLA2‐IIA indicated positive cells in the penumbral area similar to the GFAP‐positive astrocytes but different from the isolectin B4‐positive microglial cells. Confocal microscopy further confirmed immunoreactivity of sPLA2‐IIA in reactive astrocytes but not in microglial cells. Taken together, these results demonstrate for the first time an up‐regulation of the inflammatory sPLA2‐IIA in reactive astrocytes in response to cerebral ischemia–reperfusion.
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