Induction of secretory phospholipase A2 in reactive astrocytes in response to transient focal cerebral ischemia in the rat brain.
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.
Lin
Teng-Nan
TN
Neuroscience Program, Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Wang
Qun
Q
Simonyi
Agnes
A
Chen
Jean-Ju
JJ
Cheung
Wai-Mui
WM
He
Yong Y
YY
Xu
Jan
J
Sun
Albert Y
AY
Hsu
Chung Y
CY
Sun
Grace Y
GY
D000818:Animals; D001253:Astrocytes / Q000201:enzymology* / Q000473:pathology; D001921:Brain / Q000098:blood supply / Q000201:enzymology* / Q000473:pathology; D051546:Cyclooxygenase 2; D003600:Cytosol / Q000201:enzymology; D004195:Disease Models, Animal; D018450:Disease Progression; D004790:Enzyme Induction; D005904:Glial Fibrillary Acidic Protein / Q000235:genetics; D054501:Group II Phospholipases A2; D007150:Immunohistochemistry; D002546:Ischemic Attack, Transient / Q000201:enzymology* / Q000473:pathology; D007527:Isoenzymes / Q000235:genetics; D008297:Male; D009474:Neurons / Q000201:enzymology / Q000473:pathology; D010741:Phospholipases A / Q000096:biosynthesis* / Q000235:genetics; D054467:Phospholipases A2; D011451:Prostaglandin-Endoperoxide Synthases / Q000235:genetics; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D020318:Rats, Long-Evans
D005904:Glial Fibrillary Acidic Protein; D007527:Isoenzymes; D012333:RNA, Messenger; D051546:Cyclooxygenase 2; D011451:Prostaglandin-Endoperoxide Synthases; D010741:Phospholipases A; D054501:Group II Phospholipases A2; D054467:Phospholipases A2