简介：ObjectivesTotestthehypothesesthatbonemorphogeneticprotein(BMP)signalingpathwaycomponentsareexpressedinarterialendothelialcells(ECs)andthatBMPsignalinginfluencesendothelialcell(EC)proliferation.MethodsWeusedcellcultureandRT-PCRtodeterminedmRNAexpressionofBMPreceptors(BMPR)-IA,-IB,andII,Smads1,4,5,6,and7,andinculturedhumancoronaryarteryECsatbaselineandafterstimulationwithBMP2(300ng/mLfor6hr),non-radioactivecellproliferationtoexaminecellproliferation.ResultsProteasomeinhibitionhasbeenpreviouslyshowntoenhanceBMPsignalingbypreventingdegradationofBMPpathwaycomponents.Therefore,identicalexperimentswerealsoperformedinthepresenceoftheproteasomeinhibitorepoxomicin.ECsexpressedmRNAforBMPRsIAandII,Smads1,4,5,6,7,andstimulationwitheitherBMP2orepoxomicinresultedinasignificantincreaseinECproliferationmeasuredafter48hoursinadose-dependentfashion.Proliferationwasaccompaniedbyamarkedincreaseinproliferatingcellnuclearantigen(PCNA)expression.Toxicitywasobservedathighdosesofepoxomicin.ConclusionsAllmajorBMPsignalingmoleculesareexpressedbyvascularECsandexpressionoftheseareaffectedbybothBMP2andepoxomicin.BMP2mayregulateECproliferation,suggestingapossibleroleinvascularhomeostasisandvascularpathologiesinvolvingECdenudationorproliferation.

简介：AlthoughanassociationbetweenthegroupAbetahemolyticstreptococcusandrheumaticfeverhasbeenrecognizedformorethanhalfacentury,manyimportantissuesaboutthisrelationshipremainincompletelydefined.Theinitiatingpharyngealthroatinfectionand

简介：ObjectivesToinvestigatetheeffectsofatorvastatinonthemRNAexpressionofintercellularadhesionmolecule-1(ICAM-1)andvascularcelladhesionmolecule-1(VCAM-1)activatedbyTNF-αinculturedhumanumbilicalveinendothelialcells(HUVEC).MethodsandResultsLacticdehydrogenase(LDH)activityintheculturemediaincreasedwhenHUVECwereincubatedwithTNF-α,suggestingacytotoxiceffectofTNF-αonHUVEC.ThemRNAexpressionofICAM-1andVCAM-1increasedinHUVECincubatedwith10μg/LTNF-αandreachedpeakinHUVECincubatedwith30μg/LTNF-α.ThemRNAexpressionofICAM-1andVCAM-1inHUVECincubatedwith30μg/LTNF-αbegantoincreaseat6h,reachedpeakat48h,andkeptaplateauuntil72h.Atorvastatindose-dependentlyinhibitedthemRNAexpressionsofICAM-1andVCAM-1activatedbyincubatingHUVECwith30μg/LTNF-αfor48hours.ConclusionsAtorvastatinmightstabilizeplaqueanddeceleratetheprocessofASbyinhibitingthemRNAexpressionsofICAM-1andVCAM-1.

简介：Thisexperimentusedwhole-cellpatch-clamptechniquetoinvestigatethecourseofrecoveryfromuse-dependentblockofNa+channels(Nav1.5)inhumanembryonickidney(HEK)cells,onwhichtoverifytheeffectsofvolatileoilofNardostachychinesisBatal(Gansong).MethodsTwopulsesgeneratedbycomputerfollowedbyarecoverypulseandatestpulse,theintervaldurationbetweenthetwopulsesvariedfrom16msto1s,andholdingpotentialis-80mVto-140mV.ThepeakNa+currentforagivenrecoverytimewasnormalizedtothefullyrecoveredpeakcurrent,andthenormalizedvaluewastheplotasafunctionoftherecoverytimetostudytheeffectsof3ppmconcentrationGansongvolatileoilonrecoveryfromuse-dependentblockofNav1.5inHEK.ResultsItshowedthatGansonggroup,comparingwithcontrolgroup,delayedthetimecoursesofrecoveryfromuse-dependentblock[(33.2±5.77)msforcontrolgroupand(52.5±6.08)msfor3ppmGansonggroup,P<0.05].InthepresenceofGansong,inhibitionoftheNa+currentwasenhancedbyincreasingfrequencyofdepolarizingpulsefrom56.5msto16ms.Inthecontrolgroup,thetimecourseofrecoveryshowedthatrecoverystartedat19.5msandfinishedby36.5ms.InthepresenceofGansong,thetimecourseofrecoveryshowedthatrecoverystartedat36.5msandfinishedby56.5ms.Na+currentsrecoveredfromtheuse-dependentblockvaryingwithholdingpotential(holdingpotential-dependent).ConclusionsTheresultssuggestedthatNa+currentsrecoveredfromtheuse-dependentblockcorrelatedwithpersistenttime,holdingpotential.TheGansongvolatileoilhasinhibitiveeffectontheNa+currentrecovery.