1 / 3

human cardiomyocytes

Cardiomyocytes are derived from the whole heart (of a single donor) that has been dissociated into single cells and cultured using differential adhesion. Learn more from https://www.creative-bioarray.com/Human-Cardiomyocytes-CSC-C2847-item-39324.htm

creativebioarray22
Download Presentation

human cardiomyocytes

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. HowtoAvoidHumanCardiomyocyteHypertrophy WhatisHumancardiomyocytes? Humancardiomyocyteshavehorizontalstripes,whichareinnervatedbyvegetativenerves.They belongtoinvoluntarymuscleswithhorizontalstripesandhavetheabilityofexcitatory contraction.Shortcylindrical,branching,withanucleusinthecenterofthecell,usuallyone.The endsofthemyocardialfiberbranchescanbeconnectedtoeachothertoformthemyocardial fibernetwork.Inabroadsense,myocardialcellsincludespeciallydifferentiatedmyocardialcells thatcomprisesinusatrialnode,intraventricularbundle,atrioventricularjunction,atrioventricular bundle(i.e.,hissbundle)andpurkinjefiber,aswellasgeneralatrialmuscleandventricular muscleworkingcells. HowtoAvoidHumanCardiomyocyteHypertrophy 1.Thedirecteffectofmechanicalstimulationisprolongedpressureand/orvolumeoverload. Thestressontheventricularwallincreases,leadingtocardiachypertrophy.Wholeexperiment showsthatcardiachypertrophycanoccurwhentheheartisstimulatedbyload.Mechanical stimulationcanleadtocardiachypertrophybypromotingproteinsynthesisor/orprotein degradation.Themechanismisasfollows:(1)whenintracellularCAMPincreasesinthepulsating orcardiacarrest,theaorticpressureincreasesfrom7.98kPa(60mmHg)to15.96kPa(118mmHg), proteinsynthesis,nucleoproteinformation,CAMPcontentandcamp-dependentproteinkinase activityincrease,suggestingthatincreasedarterialpressurecanaccelerateproteinsynthesis throughthecamp-dependentmechanism.(2)intracellularphosphoinositideincreasedPortzeret al.reportedthat,whenaorticstenosiscausedleftventricularhypertrophy,theactivityof cytoplasmicproteinkinase(PKC)inhypertrophicmyocardiumincreasedby15%comparedwith thecontrolgroup,andtheactivityofmembranePKCincreasedby40%.Thissuggeststhatthe activationofphospholipaseCmaybethereasonwhymyocardialstretchincreasesthecontentof phosphoinositideinmyocardium.(3)increasedexpressionofproto-oncogenescanbeobserved intheearlystageofmyocardialhypertrophycausedbyexcessivepressureload.(4)increased

  2. expressionofactinandmyosingeneswhenculturedmyocardialcellswerecontinuouslyexpressionofactinandmyosingeneswhenculturedmyocardialcellswerecontinuously stimulatedbystretch,theexpressionof-mhcand-actingenesincreased.(5)othercalciumion channels,sodiumioninfluxandintracellularalkalinityratiocanplayimportantregulatoryrolesin myocardialhypertrophyinducedbystretchstimulation. 2.Chemicalstimulationofhumoralfactorsmayalsopromotecellhypertrophyorproliferation. (1),norepinephrine(NE),animalexperimentsshowthatthelong-terminjectionofhypertension doseNEmayinducemyocardialhypertrophy,themyocardialhypertrophymaymainlythrough alpha1-Rworks,somescholarsalsowilljointherestofthemyocardialcellculturecanbefound thatmycgenetranscriptionis5~10times,andpromotemyocardialhypertrophy,thereaction canbenon-specific,alpha1receptorantagonistblockingcanstrengthenbyproteinkinaseC, activatorPNAincreaseNEbyalphareceptors,activationofphosphatidylinositol,proteinkinaseC system,activationofoncogeneexpression.(2)androgenCabral,etcinratstoinduceneurogenic hypertensionafterbaroreceptornervefoundthatmaleratssignificantlyhigherthanthatof females,leftventricularweight/bodyweightratiototestosteronecancausesimilarmale neurogenichypertensionleftventricularmyocardialhypertrophyinrats,andgiveestradiolcan inhibitleftventricularweightincrease,itsmechanismisstillnotclear,mayberelatedtocancer gene.(3)angiotensinⅡ(AngⅡ)AngⅡAT1andAT2receptorspointstwosubtypes,AT1 receptorandmyocardialpositiveinotropicandchronotropicactionandthegrowthofthe myocardialcellhypertrophyrelatedtoAngⅡaddtothemyocardialcellculture,cfos,c-jun,c- myeprotocarcinogenicgeneexpression,suchasstrengtheningrapidly,andleadtoincreased proteinsynthesis,theinducedmyocardialhypertrophy.AngⅡcanalsocauseangiotensinoriginal geneandtransforminggrowthfactorbeta1,promptingthemyocytehypertrophy,thereaction canbeAngⅡAT1receptorblockersblock,canalsobePKC,promptAngⅡbyAT1receptor activationinositolphosphateester-proteinkinaseCsystem,activatesprotocarcinogenicgene expression.(4)endothelin(ET)wasisolatedfrompigaorticendothelialcellsbyYangisawaETalin 1988.ETplaysaroleinregulatingcellproliferationbybindingtoETreceptorsontargetcells.ET receptorsaredividedintoETA,ETB,ETC.CardiovascularmusclecellsarerichinETA,andETAcan causemyocardialhypertrophy,possiblybyincreasingtheexpressionoflightbond2,alpha-actin, troponin,andheavychainmRNAofalphaandbetamyosin.IthasbeenreportedthatETAmay alsoplayaroleinmyocardialhypertrophycausedbyNEinthebody.(5)growthhormone(GH) andinsulin-likegrowthfactor(TGF)Antonioetal.observedtheeffectsofGHandTGF1onthe cardiovascularsystemofrats,andfoundthatthemyocardiumwasthetargetorganofGHand igf-1,andexogenousGHandigf-1couldcausehypertrophyofthemyocardiumofnormaladult rats.Theincreasedvolumeandpressureloadcanenhancethegeneexpressionofcardiacigf-1.GH andigf-1mayalsofunctionindirectlythroughinsulinmetabolismortheadrenalinsystem.(6) interleukin6(il-6)andmastcellfactor(ct-1)keikoetal.foundthatwhenmyocardialcellswere stimulatedbyhypoxia,reperfusionandotherfactors,theycouldsecretealargeamountofil-6, whichwasrelatedtomyocardialhypertrophy.Il-6,asaligand,bindstotheil-6receptortoform homodimerGP130,whichactivatesthetyrosinekinaseandaseriesofreactionssuchas ras-paf-mapkinase,promotingthetranscriptionactivityofcellgenes.Ct-1isaproteinwith molecularweightof21.5KDaisolatedfromthesupernatantofmouseembryonicstemcells duringdifferentiationinduction.Ithasbeenreportedthatcardiomyocytesalsoproducect-1and alsoaffectintracellularsignalingthroughGP130.TheroleofCT-1stimulatemyocytehypertrophy thanAngⅡandETwerestronger,CT-1Mayalsomakethemyocardialcellcfos,c-junandANP,

  3. mRNAexpressionincreased,thatCT-1genetranscriptionactivationandnervecells.mRNAexpressionincreased,thatCT-1genetranscriptionactivationandnervecells. AboutCreativeBioarray CreativeBioarrayisaninnovativebiotechnologycompanywhosemissionfocuseson developinguniquetechnologiesthatprovideglobalscientistswithhighqualityproductsand satisfactoryservicestofacilitatetheinvestigationoflifescienceresearches. Weprovideawiderangeofhighqualitynormalhumanandanimalcells,cellculturemedium andreagents,FISHprobes,tissuearrays,microorganismsandequipments.Inaddition,we alsoofferseriesofrelatedservicesincludingcellservices,biosampleservicesandhistology servicesfortheresearchertomaketheirprojectbetterandfaster.

More Related