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) Protein Expression
1 Department of Environmental Health Sciences, University of Michigan, Ann Arbor, MI, USA
2 Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, University of Michigan, Ann Arbor, MI, USA
3 Department of Pathobiology, University of Tennessee, Knoxville, TN, USA
* To whom correspondence should be addressed. E-mail: pmancuso{at}umich.edu.
Leptin is a hormone secreted by adipocytes in correlation with total body fat mass. In addition to regulating energy homeostasis, leptin modulates immune functions such as macrophage phagocytosis and cytokine synthesis. Previously, we reported defective leukotriene synthesis in macrophages from leptin-deficient mice that could be restored with exogenous leptin. In the present study, we utilized macrophages from normal rodents to explore the mechanism by which leptin could enhance cellular leukotriene synthesis. Leptin pretreatment of either rat alveolar or murine peritoneal macrophages for 16 h dose-dependently increased the synthesis of leukotriene B4 and cysteinyl-leukotrienes in response to calcium ionophore or the particulate zymosan. Leptin also enhanced calcium ionophore stimulated release of free arachidonic acid. Calcium-dependent and -independent arachidonoyl-selective phospholipase activities in macrophage lysates were likewise increased following leptin treatment. Immunoblot
analysis of leptin-treated cells revealed that Group IVC iPLA2 (cPLA2
) protein
expression increased approximately 80%. These data demonstrate for the first time that
PLA2 activity and cPLA2 protein levels in alveolar macrophages represent targets for
upregulation by leptin and provide previously unrecognized mechanisms by which this hormone can promote inflammatory responses.
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