Membrane lipid interactions in intestinal ischemia/reperfusion-induced Injury |
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Authors: | Emily Archer Slone Sherry D. Fleming |
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Affiliation: | 1. College of Veterinary Medicine, Kansas State University, Manhattan, KS 66506, USA;2. Division of Biology, Kansas State University, Manhattan, KS 66506, USA |
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Abstract: | Ischemia, lack of blood flow, and reperfusion, return of blood flow, are a common phenomenon affecting millions of Americans each year. Roughly 30,000 Americans per year experience intestinal ischemia-reperfusion (IR), which is associated with a high mortality rate. Previous studies of the intestine established a role for neutrophils, eicosanoids, the complement system and naturally occurring antibodies in IR-induced pathology. Furthermore, data indicate involvement of a lipid or lipid-like moiety in mediating IR-induced damage. It has been proposed that antibodies recognize exposure of neo-antigens, triggering action of the complement cascade. While it is evident that the pathophysiology of IR-induced injury is complex and multi-factorial, we focus this review on the involvement of eicosanoids, phospholipids and neo-antigens in the early pathogenesis. Lipid changes occurring in response to IR, neo-antigens exposed and the role of a phospholipid transporter, phospholipid scramblase 1 will be discussed. |
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Keywords: | AA, arachidonic acid ATP, adenosine tri-phosphate β2-GPI, beta2-glycoprotein 1 cAMP, cyclic adenosine mono-phosphate Cox, cyclooxygenase cPLA2, cytosolic phospholipase A2 CR2, complement receptor 2 ESI-MS/MS, electrospray ionization-tandem mass spectrometry HR, hypoxia re-oxygenation HUVEC, human umbilical vein endothelial cells Ig, immunoglobulin IR, ischemia reperfusion Lox, lipoxygenase LTB4, leukotriene B4 MBL, mannose binding lectin miRNA, micro ribonucleic acid mTOR, mammalian target of rapamycin MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide NFκB, nuclear factor kappa-light-chain-enhancer of activated B cells PA, phosphatidic acid PC, phosphatidylcholine PE, phosphatidylethanolamine PGE2, prostaglandin E2 PGF2α, prostaglandin F2 alpha PGI2, prostaglandin I2 PI, phosphatidylinositol PLA2, phospholipase A2 PLSCR, phospholipid scramblase PS, phosphatidylserine Rag, recombination activating gene sCR1, soluble complement receptor type 1 TxB2, thromboxane B2 |
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