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논문분류	춘계학술대회 초록집
제목	Orai1 channel inhibition protects podocyte injury in BTBR ob/ob diabetic mouse Kidneys
저자	Yooujin Kwak
출판정보	2023; 2023(1):
키워드
초록	Objectives: Diabeticnephropathy(DN)isarepresentativediseasethataccountsforabouthalfofchronickidneydisease(CKD).RenalfibrosisisknowntobethemostimportantpathologicalchangeinDN.DeregulationoftheCa2+signalhasbeenimplicatedinthedevelopmentofDN,directlyand/orindirectly.Store-operatedCa2+entry(SOCE)istheprimaryCa2+entrymechanisminthenon-excitablecellsincludingpodocytesandisproposedasapotentialtherapeutictargetforDN.Recently,itisreportedthattheblockadeofSOCEprotectspodocytopathybyrestoringitsstructuralandfunctionalchanges.Here,weexaminedwhethertheOrai1inhibitorexertstherapeuticeffectsinleptin-deficientBTBRob/obmouse,awell-establishedtypeIIdiabeticmousemodel. Methods: Orai1inhibitor(GSK7975A)wasintroducedviaanosmoticminipumpfor4weeks,andasalineosmoticpumpwasusedforthevehicle.Glomerulartuftareaandmesangialmatrix(byMethenaminesilverstain),andpodocytedensity(byimmunohistochemicalstainingwithWT1)werequantifiedbyimageanalyzerandcomparedamonggroups.Glomerularbasementmembrane(GBM)thicknesswasanalyzedbyelectronmicroscopy. Results: Orai1inhibitorsignificantlyreducedmesangialmatrixintheBTBRob/obmicecomparedwiththatofsaline-treatedoruntreatedBTBRob/obmice.PodocytedensitywasdiminishedinBTBRob/obmice,andwassignificantlyamelioratedbyOrai1inhibitoradministration(Fig.1).Furthermore,GBMthicknesswasalsodecreasedinOrai1inhibitor-treatedBTBRob/obmicecomparedtothatofsalineinfusion. Conclusions: Takentogether,ourdatademonstratethattheblockadeofOrai1activitymayrestorethepathologicchangesofDNinBTBRob/obmouse,andproposedOrai1asanoveltherapeutictargetforDN.
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