Induction of secretory phospholipase A₂ in reactive astrocytes in response to transient focal cerebral ischemia in the rat brain

<jats:title>Abstract</jats:title><jats:p>Although mRNA expression of group IIA secretory phospholipase A<jats:sub>2</jats:sub> (sPLA<jats:sub>2</jats:sub>‐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 sPLA<jats:sub>2</jats:sub>‐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 sPLA<jats:sub>2</jats:sub>‐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. <jats:italic>In situ</jats:italic> hybridization localized the early‐phase increase in sPLA<jats:sub>2</jats:sub>‐IIA mRNA to the affected ischemic cortex and the late‐phase increase to the penumbral area. Besides sPLA<jats:sub>2</jats:sub>‐IIA mRNA, glial fibrillary acidic protein (GFAP) and cyclo‐oxygenase‐2 mRNAs, but not cytosolic PLA<jats:sub>2</jats:sub>, also showed an increase in the penumbral area at 3 days after ischemia–reperfusion. Immunohistochemistry of sPLA<jats:sub>2</jats:sub>‐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 sPLA<jats:sub>2</jats:sub>‐IIA in reactive astrocytes but not in microglial cells. Taken together, these results demonstrate for the first time an up‐regulation of the inflammatory sPLA<jats:sub>2</jats:sub>‐IIA in reactive astrocytes in response to cerebral ischemia–reperfusion.</jats:p>