Aldolase B Knockdown Prevents High Glucose-Induced Methylglyoxal Overproduction and Cellular Dysfunction in Endothelial Cells 英文参考文献.docVIP

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Aldolase B Knockdown Prevents High Glucose-Induced Methylglyoxal Overproduction and Cellular Dysfunction in Endothelial Cells 英文参考文献.doc

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Aldolase B Knockdown Prevents High Glucose-Induced Methylglyoxal Overproduction and Cellular Dysfunction in Endothelial Cells 英文参考文献

AldolaseBKnockdownPreventsHighGlucose-Induced MethylglyoxalOverproductionandCellularDysfunction inEndothelialCells JianghaiLiu1,TimothyChun-PingMak1,AliBanigesh1,KaushikDesai1,RuiWang2,LingyunWu1,3* 1Department of Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada, 2Department of Biology, Lakehead University, ThunderBay,Ontario,Canada,3DepartmentofHealthSciences,LakeheadUniversityandThunderBayRegionalResearchInstitute,ThunderBay,Ontario,Canada Abstract Weusedculturedendothelialcellsasamodeltoexaminewhetherup-regulationofaldolaseBandenhancedmethylglyoxal (MG) formation play an important role in high glucose-induced overproduction of advanced glycosylation endproducts (AGEs), oxidative stress and cellular dysfunction. High glucose (25mM) incubation up-regulated mRNA levels of aldose reductase (an enzyme converting glucose to fructose) and aldolase B (a key enzyme that catalyzes MG formation from fructose) and enhanced MG formation in human umbilical vein endothelial cells (HUVECs) and HUVEC-derived EA. hy926cells.Highglucose-increasedMGproductioninEA.hy926cellswascompletelypreventedbysiRNAknockdownof aldolaseB,butunaffectedbysiRNAknockdownofaldolaseA,anenzymeresponsibleforMGformationduringglycolysis.In addition, inhibition of cytochrome P450 2E1 or semicarbazide-sensitive amine oxidase which produces MG during the metabolism of lipid and proteins, respectively, did not alter MG production. Both high glucose (25mM) and MG (30, 100mM)increasedtheformationofN(e)-carboxyethyl-lysine(CEL,aMG-inducedAGE),oxidativestress(determinedbythe generation of oxidized DCF, H2O2, protein carbonyls and 8-oxo-dG), O-GlcNAc modification (product of the hexosamine pathway),membraneproteinkinaseCactivityandnucleartranslocationofNF-kBinEA.hy926cells.However,theabove metabolicandsignalingalterationsinducedbyhighglucosewerecompletelypreventedbyknockdownofaldolaseBand partially by application of aminoguanidine (a MG scavenger) or alagebrium (an AGEs