Sialoglycosylation of RBC in Visceral Leishmaniasis Leads to Enhanced Oxidative Stress, Calpain-Induced Fragmentation of Spectrin and Hemolysis 英文参考文献.docVIP

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Sialoglycosylation of RBC in Visceral Leishmaniasis Leads to Enhanced Oxidative Stress, Calpain-Induced Fragmentation of Spectrin and Hemolysis 英文参考文献.doc

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Sialoglycosylation of RBC in Visceral Leishmaniasis Leads to Enhanced Oxidative Stress, Calpain-Induced Fragmentation of Spectrin and Hemolysis 英文参考文献

SialoglycosylationofRBCinVisceralLeishmaniasisLeads toEnhancedOxidativeStress,Calpain-Induced FragmentationofSpectrinandHemolysis SajalSamanta1,AnganaGhoshal1¤,KaushikBhattacharya1,BibhutiSaha2,PeterWalden3, ChitraMandal1* 1Cancer Biology and Inflammatory Disorder Division; CSIR-Indian Institute of Chemical Biology, Kolkata, India, 2Department of Tropical Medicine, School of Tropical Medicine,Kolkata,India,3DepartmentofDermatology,Charite′-Universita¨tsmedizin Berlin,HumboldtUniversityBerlin,Germany Abstract Visceral leishmaniasis (VL) caused by the intracellular parasite Leishmania donovani accounts for an estimated 12 million cases of human infection. It is almost always associated with anemia, which severely complicates the disease course. However,thepathologicalprocessesleadingtoanemiainVLhavethusfarnotbeenadequatelycharacterizedtodate.In studyingtheglycosylationpatternsofperipheralbloodcellswefoundthattheredbloodcells(RBC)ofVLpatients(RBCVL) expresseight9-O-acetylatedsialoglycoproteins(9-O-AcSGPs)thatarenotdetectedintheRBCofhealthyindividuals(RBCN). Atthesametime,thepatientshadhightitersofanti-9-O-AcSGPIgGantibodiesintheirsera.Thesetwoconditionsappearto belinkedandrelatedtotheanemicstateofthepatients,asexposureofRBCVLbutnotRBCNtoanti-9-O-AcSGPsantibodies purifiedfrompatientseratriggered aseriesof responses.Theseincludedcalcium influxvia theP/Q-typebut notL-type channels, activation of calpain I, proteolysis of spectrin, enhanced oxidative stress, lipid peroxidation, externalization of phosphatidyl serine with enhanced erythrophagocytosis, enhanced membrane fragility and, finally, hemolysis. Taken together,thisstudysuggeststhattheenhancedhemolysisislinkedtoanimpairmentofmembraneintegrityinRBCVLwhich ismediatedbyligand-specificinteractionofsurface9-O-AcSGPs.Thisaffordsapotentialexplanationforthestructuraland functionalfeaturesofRBCVLwhichareinvolvedinthehemolysisrelatedtotheanemiawhichdevelopsinVLpatients. Citation:SamantaS,GhoshalA,BhattacharyaK,SahaB,