简介:BackgroundH9c2celllineismononucleatedmyoblastderivedfromembryonicrathearttissue.ActivitiesofTGF-β1,MMP-2andMMP-9increaseinH9c2cellsaftertreatmentwithfibrosisstimuli.MicroRNA(miRNA),akindofendogenoussmallnon-codingRNA,participatesincardiacfibrosis.Inthepresentstudy,expressionsoffibrosis-relatedgenesandmicroRNAsinTGF-β1treatedH9c2cellswereinvestigated.MethodsExpressionsoffibrosis-associatedgenes,includingCol3a1,α-SMA,FN1,CTGFandTSP-1,weremeasuredinTGF-β1treatedH9c2cellsbyquantitativereversetranscriptionandPCR(qRTPCR).Levelofα-SMAinH9c2cellswasdemonstratedbyfluorescenceimmunohistochemistry(FIHC)assay.ExpressionsofmaturemiR-16,-21a,-29binH9c2cellsweredeterminedbyqRT-PCRassay.ActivationsofSmad3andNF-kBsignalinginTGF-β1-treatedH9c2cellswerestudiedbydualluciferaseassay.ExpressionsofCol3a1,α-SMA,FN1,CTGFandTSP-1weredetectedinH9c2cellswithadenovirus-mediatedoverexpressionofmiR-21a.ResultsqRT-PCRassayshowedthatα-SMA,FN1,CTGF,TSP-1,butnotCol3a1,wereup-regulatedinTGF-β1treatedH9c2cells.FIHCresultalsorevealedthatα-SMAwasincreasedinTGF-β1-treatedH9c2cells.Consistently,dualluciferaseassayshowedthatSmad3andNF-kBsignalingproteinswereactivatedinTGF-β1-treatedH9c2cells.miR-21a,butnotmiR-16and-29b,wassignificantlyup-regulated.Additionally,over-expressionofmiR-21asignificantlyincreasesmRNAexpressionsofα-SMA,FN1,CTGFandTSP-1inH9c2cells.ConclusionsMiR-21aisup-regulatedinTGF-β1treatedH9c2cells,andmaycontributetoup-regulationsoffibrosis-associatedgenes.
简介:BackgroundTheremaybedysregulationofcirculatingmicroRNAsinacutemyocardialinfarction(AMI),whichisanaging-relatedprocess.However,thedifferencebetweenyoungandelderlypeopleinexpressionlevelofcirculatingmiR-21inAMIpatientshasnotbeeninvestigated.MethodsThestudyincluded72consecutivepatientswithAMI.ThegroupIconsistedof43patientsagedequaltoorabove65yearsandthegroupIIconsistedof29patientsagedequaltoorbelow45years.Real-timeRT-PCRwasappliedtodetectserummiR-21expressionlevelsatthetimeofmechanicalreperfusionand12h,D1,D3andD7afterPCI,respectively.ResultsTheexpressionlevelofmiR-21inAMIpatientsincreasedmarkedly12hafterPCIandreachedthepeakatD1afterPCIinbothgroups.TherewasnodifferenceofmiR-21expressionbetweenGroupⅠandⅡatthetimeofmechanicalreperfusion(5.12±0.73vs.4.98±0.87)andD7afterPCI(1.28±0.75vs.1.94±0.89),However,groupⅠpatientsexhibitedhighermiR-21expressionlevelthangroupⅡat12h(7.96±0.78vs.4.23±0.77,P<0.05),D1(9.32±0.89vs.6.12±0.92,P<0.05)andD3(4.78±0.91vs.2.97±0.77,P<0.05)afterPCI,respectively.ConclusionOurdatarevealanincreaseofmiR-21inpatientswithAMImaybeamechanismofmyocardialischemiareperfusioninjury.TheexpressionofmiR-21wasrelatedtothedevelopmentandprogressionofAMI,andthereisanage-relatedchangeintheexpressionofmiR-21inacutemyocardialinfarctionpatients.
简介:目的探讨中心分流术在治疗重症法洛四联症(tetralogyofFallot,TOF)中的应用,评价其手术效果.方法回顾性分析21例应用Gore-Tex管(膨体聚四氟乙烯人工血管)行升主动脉到主肺动脉中心分流手术的TOF患者的临床资料.着重分析手术方法、手术结果及术后随访.结果手术死亡2例,术后3d内分别死于低心排血量综合征和肺水肿,病死率9.5%(2/21).12例于术后6个月~24个月内行二期手术根治,无死亡患者.根治术中无发现Gore-Tex管堵塞者.术后动脉血氧饱和度及动脉血氧分压比术前显著改善[90.0%±4.0%比60.0%±5.05%,P<0.01;(53.4±14.1)mmHg比(42.2±8.8)mmHg,P<0.01].12例患者二期根治术时与中心分流术时比较,左心室及肺动脉发育均明显改善.结论中心分流术是改善重症法洛四联症症状、体征可供选择的手术方式,是重症法洛四联症根治术的一种良好的分期手术方式.
简介:目的探讨甲型H1N1流感患者心脏损害的特点。方法回顾性研究分析2009年7月至2010年1月期间确诊为甲型H1N1流感患者172例的临床资料,所有患者根据病情分为轻症组,重症组,危重症组,并收集非甲型H1N1流感患者21例作为对照。大部分患者接受分子生物学检测磷酸肌酸激酶,磷酸肌酸激酶同工酶,高敏C反应蛋白,并接受胸部X线摄片检查,计算心胸比。结果甲型H1N1流感多发生于青壮年患者,轻症患者较重症患者更年轻(P<0.05)。在危重症患者中,磷酸肌酸激酶,磷酸肌酸激酶同工酶,高敏C反应蛋白和心胸比均较其他组高(P<0.05或P<0.01)。1例死于心肌损害。结论与既往研究相符,2009甲型H1N1流感可以导致心肌损害,特别是在危重症患者中心肌损害较显著,从而将导致心脏扩大等损害,导致死亡率升高。
简介:ObjectivesToexploretheprotectiveeffectofirbesartan(Irb)undertheinterferencewithangiotensinⅡ(AngⅡ)onABCA1.MethodsElectronmicroscopywasusedtodetectthemorphousoffoamcells.TheexpressionofABCA1mRNAanditsproteinweredeterminedbyRT-PCRandWesternblotting,respectively.Thevarianceofcellularcholesterolcontentwasmeasuredbyzymochemistryvia-fluorospectrophotometer.ResultsApositivefacilitativeeffectofAngⅡontheformationoffoamcellswasobserved.TotalcholesterolwasincreasedsignificantlybyAngⅡ,theexpressionofABCA1wasdown-regulatedobviouslybyAngⅡ;IrbcouldprotectABCA1againstthelesionofAngⅡ;TotalcellularcholesterolcontentwasreducedsignificantlyinIrb+AngⅡgroup;However,considerablealterationaboutthecholesterolcontentandtheexpressionofABCA1werenotobservedinIrbgroupwithoutincubationwithAngⅡ.ConclusionsIrbcouldprotectABCA1againstthelesionofAngⅡ,whichmaycontributetoitsanti-atheroscleroticproperties.
简介:T1mappingusingcardiovascularmagneticresonance(CMR)introducesnoveltechniquesformyocardialtissuecharacterizationtodetectandquantifydiseaseprocessesoccurringatthemicroscopiclevel.EventhoughT1mappinghaslimitedspatialresolution,cellularandmolecularchangesoccurringwithineachvoxelcanaffecttheaggregateT1signalrenderingthemquantifiable.TheestimatedT1-basedparametersquantifiedona“map”demonstratethespatiallocalizationofthesechangeswherebyeachpixelexpressesthequantitativevalueofthatparameter.Thisquantificationpermitsdetectionofdiffusediseaseevenifitisnotdirectlyvisible.Ratherthanrelyingonnonspecificfunctionalmeasures,T1mappingfocusesonintrinsicchangesofmyocardialcompositionthatadvancesunderstandingaboutspecificdiseasepathways.Thesechangesinmyocardialtissuecompositioninformdiagnosisandprognosis.T1mappingencompassestwokeyparameters:native(i.e.,precontrast)T1andextracellularvolumefraction(ECV)derivedfromadditionalpostcontrastT1andbloodT1measurements.Theseadvancesintroducenewtoolstodetectfocalanddiffusemyocardialderangementsoccurringincardiacdiseasethatcanbeotherwisedifficulttodetect.T1andECVmappingfosterprecisionmedicineandpersonalizedcare,promisingtoimprovepatientoutcomesthroughtargetedtherapy.CapitalizingontheopportunitiesintroducedbyT1mappingandECVrequiresfurtherinvestigation.