Reduced fertility and postischaemic brain injury in mice deficient in cytosolic phospholipase A2

Joseph V. Bonventre (), Zhihong Huang, M. Reza Taheri, Eileen O'Leary, En Li, Michael A. Moskowitz and Adam Sapirstein
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Joseph V. Bonventre: Medical, Massachusetts General Hospital, Neurosurgery and Anesthesia, and Harvard Medical School
Zhihong Huang: Neurosurgical, Massachusetts General Hospital, Neurosurgery and Anesthesia, and Harvard Medical School
M. Reza Taheri: Medical, Massachusetts General Hospital, Neurosurgery and Anesthesia, and Harvard Medical School
Eileen O'Leary: Medical, Massachusetts General Hospital, Neurosurgery and Anesthesia, and Harvard Medical School
En Li: Cardiac, Massachusetts General Hospital, Neurosurgery and Anesthesia, and Harvard Medical School
Michael A. Moskowitz: Neurosurgical, Massachusetts General Hospital, Neurosurgery and Anesthesia, and Harvard Medical School
Adam Sapirstein: Anesthesia Services, Massachusetts General Hospital, Neurosurgery and Anesthesia, and Harvard Medical School

Nature, 1997, vol. 390, issue 6660, 622-625

Abstract: Abstract Phospholipase A2 (PLA2) enzymes are critical regulators of prostaglandin and leukotriene synthesis and can directly modify the composition of cellular membranes1,2. PLA2 enzymes release fatty acids and lysophospholipids, including the precursor of platelet-activating factor, PAF, from phospholipids. Free fatty acids, eicosanoids, lysophospholipids and PAF are potent regulators of inflammation1,3,4, reproduction5,6,7 and neurotoxicity1,8,9. The physiological roles of the various forms of PLA2 are not well defined. The cytosolic form, cPLA2, preferentially releases arachidonic acid from phospholipids and is regulated by changes in intracellular calcium concentration10,11. We have now created ‘knockout’ (cPLA2−/−) mice that lack this enzyme, in order to evaluate its physiological importance. We find that cPLA2−/− mice develop normally, but that the females produce only small litters in which the pups are usually dead. Stimulated peritoneal macrophages from cPLA2−/− animals did not produce prostaglandin E2 or leukotriene B4 or C4. After transient middle cerebral artery occlusion, cPLA2−/− mice had smaller infarcts and developed less brain oedema and fewer neurological deficits. Thus cPLA2 is important for macrophage production of inflammatory mediators, fertility, and in the pathophysiology of neuronal death after transient focal cerebral ischaemia.

Date: 1997
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DOI: 10.1038/37635

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