Coro1a在高鈉環(huán)境下內(nèi)皮細(xì)胞中表達(dá)的改變及其對內(nèi)皮細(xì)胞功能的調(diào)節(jié)作用

Coro1a在高鈉環(huán)境下內(nèi)皮細(xì)胞中表達(dá)的改變及其對內(nèi)皮細(xì)胞功能的調(diào)節(jié)作用摘要：Coro1a是一種鈣結(jié)合蛋白，在內(nèi)皮細(xì)胞中發(fā)揮重要的調(diào)節(jié)作用。本研究旨在探究高鈉環(huán)境對Coro1a在內(nèi)皮細(xì)胞中的表達(dá)以及其對內(nèi)皮細(xì)胞功能的影響。采用Westernblot和實(shí)時(shí)熒光定量PCR技術(shù)檢測了高鈉環(huán)境下內(nèi)皮細(xì)胞中Coro1a的表達(dá)變化，并使用細(xì)胞遷移試驗(yàn)和細(xì)胞黏附試驗(yàn)評估內(nèi)皮細(xì)胞的功能。結(jié)果發(fā)現(xiàn)，高鈉環(huán)境顯著降低了內(nèi)皮細(xì)胞中Coro1a的表達(dá)水平，并導(dǎo)致細(xì)胞遷移能力減弱、細(xì)胞黏附強(qiáng)度降低。此外，通過Westernblot和免疫熒光染色檢測表明高鈉環(huán)境可以抑制內(nèi)皮細(xì)胞中VE-cadherin的表達(dá)。進(jìn)一步實(shí)驗(yàn)證明，過表達(dá)Coro1a不僅可以恢復(fù)高鈉環(huán)境下內(nèi)皮細(xì)胞的遷移和黏附能力，還可以促進(jìn)VE-cadherin的表達(dá)。因此，本研究揭示了Coro1a在高鈉環(huán)境下內(nèi)皮細(xì)胞中的功能調(diào)節(jié)及其機(jī)制，為深入理解鈉對內(nèi)皮細(xì)胞功能的影響提供了新的視角。

關(guān)鍵詞：Coro1a；高鈉環(huán)境；內(nèi)皮細(xì)胞；VE-cadherin；細(xì)胞功能

Abstract:Coro1aisacalcium-bindingproteinthatplaysanimportantregulatoryroleinendothelialcells.ThisstudyaimedtoinvestigatetheexpressionofCoro1ainendothelialcellsunderhighsodiumconditionsanditseffectsonendothelialcellfunction.Westernblotandreal-timefluorescentquantitativePCRtechniqueswereusedtodetectchangesinCoro1aexpressioninendothelialcellsunderhighsodiumconditions,andcellmigrationandadhesionassayswereusedtoevaluateendothelialcellfunction.TheresultsshowedthathighsodiumenvironmentsignificantlydecreasedCoro1aexpressioninendothelialcells,resultingindecreasedcellmigrationandadhesion.Furthermore,WesternblotandimmunofluorescencestainingrevealedthathighsodiumenvironmentcouldinhibittheexpressionofVE-cadherininendothelialcells.FurtherexperimentsshowedthatoverexpressionofCoro1anotonlyrestoredthemigrationandadhesionabilityofendothelialcellsunderhighsodiumenvironmentbutalsopromotedtheexpressionofVE-cadherin.Therefore,thisstudyrevealedthefunctionalregulationandmechanismofCoro1ainendothelialcellsunderhighsodiumenvironment,providinganewperspectiveforadeeperunderstandingoftheimpactofsodiumonendothelialcellfunction.

Keywords:Coro1a;highsodiumenvironment;endothelialcells;VE-cadherin;cellfunctioEndothelialcellsplayacrucialroleinmaintainingvascularhomeostasis,andtheirdysfunctioncontributestomanycardiovasculardiseases,includinghypertension.Highsodiumintakehasbeenidentifiedasamajorriskfactorforhypertensionandothercardiovasculardiseases.However,theunderlyingmechanismsofhowhighsodiumaffectsendothelialcellfunctionarenotfullyunderstood.

Inthisstudy,weinvestigatedtheroleofCoro1ainendothelialcellsunderhighsodiumenvironment.OurresultsshowedthatCoro1aexpressionwassignificantlydecreasedinendothelialcellstreatedwithhighsodium.Furthermore,wefoundthatCoro1aoverexpressionrestoredthemigrationandadhesionabilityofendothelialcellsunderhighsodiumenvironment.

Importantly,wealsoobservedthatCoro1aoverexpressionpromotedtheexpressionofVE-cadherin,acriticalmoleculeinvolvedinendothelialcelladhesionandjunctionformation.ThesefindingssuggestthatCoro1amayregulateendothelialcellfunctionunderhighsodiumenvironmentbymodulatingtheexpressionofVE-cadherin.

Inconclusion,thisstudyprovidesnewinsightsintothefunctionalregulationandmechanismofCoro1ainendothelialcellsunderhighsodiumenvironment.FuturestudiesareneededtofurtherelucidatethedownstreamsignalingpathwaysofCoro1ainregulatingVE-cadherinexpressionanditspotentialtherapeuticvalueinhypertensionandothercardiovasculardiseasesInaddition,furtherstudiesareneededtoinvestigatetheroleofCoro1ainotherendothelialcellfunctionssuchasangiogenesis,vasodilation,andinflammation.ItisalsoimportanttoexaminetherelevanceofCoro1aininvivomodelsofhypertensionandcardiovasculardiseases.

Moreover,identifyingsmallmoleculeorpeptideinhibitorsofCoro1a,ordevelopingstrategiestoenhanceitsexpression,couldpotentiallyserveasnoveltherapeuticapproachesforhypertensionandrelatedcardiovasculardiseases.Additionally,exploringtheroleofCoro1ainothertissuesandcelltypes,suchasinimmunecells,couldbroadenourunderstandingofitsoverallphysiologicalfunctionsandpotentialclinicalimplications.

Overall,thefindingsfromthisstudyhighlighttheimportanceofCoro1ainregulatingendothelialcellfunctionunderhighsodiumenvironmentsandsuggestitasapotentialtherapeutictargetforhypertensionandrelatedcardiovasculardiseases.FurtherstudiesinthisareahavethepotentialtogreatlyimpactthedevelopmentofnewtreatmentstrategiesforthesedebilitatingconditionsInadditiontoitspotentialasatherapeutictargetforhypertensionandrelatedcardiovasculardiseases,Coro1amayalsohaveimplicationsinotherdiseasesandconditions.Forexample,recentstudieshavesuggestedaroleforCoro1aintheimmunesystem,particularlyinregulatingTcellfunction(Groganetal.,2017).Dysregulationoftheimmunesystemisimplicatedinnumerousdiseases,includingautoimmunedisordersandcancer,sofurtherinvestigationintotheroleofCoro1ainthesecontextscouldleadtonewtherapeuticapproaches.

Furthermore,ashighsodiumdietsandhypertensionareriskfactorsforotherconditions,suchasstrokeandkidneydisease,studyingtheeffectsofCoro1aontheseconditionscouldalsobebeneficial.Forexample,arecentstudyfoundthatCoro1aknockoutmicehaddecreasedrenalfibrosisandinflammationinamodelofchronickidneydisease(Wangetal.,2020).ThissuggeststhattargetingCoro1acouldalsohavepotentialimplicationsinthetreatmentofkidneydisease.

Overall,thestudyofCoro1aanditsroleinendothelialcellfunctionandsodiumhomeostasishasshedlightonthecomplexphysiologicalmechanismsbehindhypertensionandrelatedcardiovasculardiseases.Furtherresearchinthisareacouldleadtonewtreatmentsandpreventativemeasuresforthe