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1、TheprotectivemechanismofheatshocktreatmentonthedisruptionoftightjunctionofendothelialcellsTzong-ShiLu1,Hsiang-WenChen3,Sheng-ILue1,Shu-JungWang1,Mei-FangKuo1,andRei-ChengYang1,2DepartmentsofPhysiology1,Pediatrics2,andMicrobiology3,GraduateInstituteofMedicine,KaohsiungMedicalUnivers
2、ity,KaohsiungCity,TAIWANAbstractEndothelialcellsplayacentralroleinthepermeationofvessels.Thevascularpermeabilityalterationismainlygovernedbytheintegrityoftheendothelialcellsandtheirtightjunctionformsacontinuouscircumferentialsealneartheapex.Disruptionofthetightjunctionbarriercontri
3、butestodiseaseprincipallybyincreasingtheinappropriateions,solutes,andwatermovementsofendothelialcells.Ourpreviousstudyindicatedthatheatshocktreatmentreducedtheproteinleakageandattenuatedthehypotensioncausedbyanaphylacticshockandmaintainedthecerebralvascularpermeabilityafterbloodbra
4、inbarrierdisruptedbyhighosmoticstress.Inthisstudy,weinvestigatedthepotentialmechanismofheatshockproteins,inducedbyheatshocktreatment,ontheprotectionoftightjunctiondisruptioninculturesendothelialcells.Tightjunctionprotein,ZO-1,wereevaluatedbyimmunochemicalstudyanditshowedthatZO-1wer
5、efaintlystainedinthespecimensafterhistaminetreatmentofnon-heatedgroup,whileitwashighlypreservedinthespecimensofheatedgroup,comparingwiththoseofnormalcontrol.Theimmunohistochemicalstudyillustratedthatheatshockprotein72(HSP72),thehighestinducibleproteinafterheatshocktreatment,wasover
6、-expressedinheatedspecimensonly.TheresultsalsoindicatedthatHSP72couldbeco-immunoprecipitatedwithZO-1inheatedspecimensonly.Inconclusion,theendothelialcellspermeabilitycouldbeprotectedbypreviousheatshocktreatment,highlypossibletheover-expressionofheatshockproteins,viathepreservationo
7、ftightjunctionproteinsandtheirintegrity.IntroductionThehomeostasismaintenanceofcirculationsystemisquiteanimportantstatusinnormalphysiologicalcondition.Generally,endothelialcellsassumeacentralroleinthepermeationofvesselsandthevascularpermeabilityalterationismainlygovernedbytheintegr
8、ityoftheendotheliumlayerof
