Prostaglandins Other Lipid Mediat
February 2022
Bone modeling can be modulated by lipid signals such as arachidonic acid (AA) and its cyclooxygenase 2 (COX2) metabolite, prostaglandin E (PGE), which are recognized mediators of optimal bone formation. Hydrolysis of AA from membrane glycerophospholipids is catalyzed by phospholipases A (PLAs). We reported that mice deficient in the Ca- independent PLAbeta (iPLAβ), encoded by Pla2g6, exhibit a low bone phenotype, but the cause for this remains to be identified.
View Article and Find Full Text PDFObesity, Type 2 Diabetes, and Metabolic Syndrome induce dyslipidemia resulting in inundation of peripheral organs with fatty acids. These not only serve as substrates for energy production, but also contribute to aberrant production of bioactive lipids. Moreover, lipid metabolism is affected in many cardiac disorders including heart failure, ischemia reperfusion injury, and others.
View Article and Find Full Text PDFMacrophages are important in innate and adaptive immunity. Macrophage participation in inflammation or tissue repair is directed by various extracellular signals and mediated by multiple intracellular pathways. Activation of group VIA phospholipase A (iPLAβ) causes accumulation of arachidonic acid, lysophospholipids, and eicosanoids that can promote inflammation and pathologic states.
View Article and Find Full Text PDFAmong the family of phospholipases A2 (PLA2s) are the Ca(2+)-independent PLA2s (iPLA2s) and they are designated group VI iPLA2s. In relation to secretory and cytosolic PLA2s, the iPLA2s are more recently described and details of their expression and roles in biological functions are rapidly emerging. The iPLA2s or patatin-like phospholipases (PNPLAs) are intracellular enzymes that do not require Ca(2+) for activity, and contain lipase (GXSXG) and nucleotide-binding (GXGXXG) consensus sequences.
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