Secretory phospholipase A(2) induces delayed neuronal COX-2 expression compared with glutamate
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Secretory phospholipase A(2) induces delayed neuronal COX-2 expression compared with glutamate. / Kolko, Miriam; Nielsen, Marianne; Bazan, Nicolas G; Diemer, Nils H.
In: Journal of Neuroscience Research, Vol. 69, No. 2, 2002, p. 169-77.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Secretory phospholipase A(2) induces delayed neuronal COX-2 expression compared with glutamate
AU - Kolko, Miriam
AU - Nielsen, Marianne
AU - Bazan, Nicolas G
AU - Diemer, Nils H
N1 - Copyright 2002 Wiley-Liss, Inc.
PY - 2002
Y1 - 2002
N2 - Agonists of the binding site for secretory phospholipase A(2) (sPLA(2)) potentiate glutamate-induced neuronal cell death in primary cell cultures and in vivo (Kolko et al. [1996] J. Biol. Chem. 271:32722; Kolko et al. [1999] Neurosci. Lett. 274:167]. Here, we tested the hypothesis that COX-2 expression participates in the brain response to sPLA(2). sPLA(2)-OS(2), a selective ligand of a neuronal sPLA(2)-binding site, was injected into the rat striatum, and early-response gene expression was monitored by in situ hybridization using (35)S-radiolabeled oligonucleotide probes and immunohistochemistry. An up-regulation of COX-2, c-fos, and c-jun, but not COX-1, was observed around the lesion as well as in the neocortex 4 hr after the injection. Hippocampal up-regulation of COX-2 was seen in dentate gyrus 8 hr after injection. When glutamate was injected, up-regulation of the early-response genes peaked after 2 hr. Our studies showed 1) that sPLA(2) selectively induced neuronal COX-2; 2) that this induction was delayed (4 hr after injection of sPLA(2)) compared with that elicited by glutamate (2 hr after injection), suggesting different signaling; and 3) that c-fos and c-jun were induced around the infarct area as soon as 2 hr after injection, but in other aspects followed a time course similar to that of COX-2. We conclude that sPLA(2) may modulate neuronal COX-2 expression through mechanisms that differ from those of glutamate-induced COX-2 expression.
AB - Agonists of the binding site for secretory phospholipase A(2) (sPLA(2)) potentiate glutamate-induced neuronal cell death in primary cell cultures and in vivo (Kolko et al. [1996] J. Biol. Chem. 271:32722; Kolko et al. [1999] Neurosci. Lett. 274:167]. Here, we tested the hypothesis that COX-2 expression participates in the brain response to sPLA(2). sPLA(2)-OS(2), a selective ligand of a neuronal sPLA(2)-binding site, was injected into the rat striatum, and early-response gene expression was monitored by in situ hybridization using (35)S-radiolabeled oligonucleotide probes and immunohistochemistry. An up-regulation of COX-2, c-fos, and c-jun, but not COX-1, was observed around the lesion as well as in the neocortex 4 hr after the injection. Hippocampal up-regulation of COX-2 was seen in dentate gyrus 8 hr after injection. When glutamate was injected, up-regulation of the early-response genes peaked after 2 hr. Our studies showed 1) that sPLA(2) selectively induced neuronal COX-2; 2) that this induction was delayed (4 hr after injection of sPLA(2)) compared with that elicited by glutamate (2 hr after injection), suggesting different signaling; and 3) that c-fos and c-jun were induced around the infarct area as soon as 2 hr after injection, but in other aspects followed a time course similar to that of COX-2. We conclude that sPLA(2) may modulate neuronal COX-2 expression through mechanisms that differ from those of glutamate-induced COX-2 expression.
KW - Animals
KW - Corpus Striatum
KW - Cyclooxygenase 1
KW - Cyclooxygenase 2
KW - Genes, fos
KW - Genes, jun
KW - Glutamic Acid
KW - Immunohistochemistry
KW - In Situ Hybridization
KW - Isoenzymes
KW - Male
KW - Membrane Proteins
KW - Neurons
KW - Phospholipases A
KW - Prostaglandin-Endoperoxide Synthases
KW - Rats
KW - Rats, Wistar
KW - Time Factors
KW - Up-Regulation
U2 - 10.1002/jnr.10288
DO - 10.1002/jnr.10288
M3 - Journal article
C2 - 12111798
VL - 69
SP - 169
EP - 177
JO - Journal of Neuroscience Research
JF - Journal of Neuroscience Research
SN - 0360-4012
IS - 2
ER -
ID: 128614405