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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

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human cardiomyocytes

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  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.

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