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Cyclooxygenase‐2 is induced globally in infarcted human brain
Author(s) -
Sairanen Tiina,
Ristimäki Ari,
KarjalainenLindsberg MarjaLiisa,
Paetau Anders,
Kaste Markku,
Lindsberg Perttu J.
Publication year - 1998
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410430608
Subject(s) - sequela , cyclooxygenase , ischemia , arachidonic acid , medicine , brain damage , brain tissue , neuroinflammation , human brain , neuroprotection , neuroscience , prostaglandin , microglia , pathology , inflammation , biology , surgery , enzyme , biochemistry
Cyclooxygenase (COX) catalyzes synthesis of prostanoids after liberation of arachidonic acid, an important biochemical sequela of cerebral ischemia that aggravates brain injury. We investigated expression of inducible COX‐2 in infarcted human brains (symptom duration, 15 hours to 18 days) and found that COX‐2 protein was present in both neuronal and glial cells throughout the brain in accord with infarct topography and duration. These results emphasize the global yet temporally regulated nature of COX‐2 induction during focal ischemia in humans, clearly different from the circumscribed acute expression reported in experimental animal models. We speculate that early induction of COX‐2 may fuel tissue damage through prostanoids and free radicals, and delayed induction in remote brain areas may promote reconstitutive processes in the face of tissue scarring and remodeling of the surviving neural networks.