TheeffectsofautophagyonvascularendothelialcellsinducedbyairbornePM2.5
摘要: ThepurposeofthisstudywastoexaminethedirecttoxicityofPM2.5collectedfromBeijingonhumanumbilicalveinendothelialcells(HUVEC).ACellCountingKit8(CCK8)assaydemonstratedthatPM2.5exposuredecreasedtheproliferationofHUVECsinadosedependentmanner.WealsofoundthatPM2.5exposureinducedautophagyinHUVECs,asevidencedby:(1)anincreasednumberofdouble-membranevesicles;(2)enhancedconversionandpunctuationofthemicrotubule-associatedproteinlightchain3(LC3);and(3)decreasedlevelsoftheselectiveautophagysubstratep62inatime-dependentmanner.Furthermore,promotingautophagyinPM2.5-exposedHUVECswithrapamycinincreasedthecellsurvivalrate,whereasinhibitingautophagyvia3-methyladeninesignificantlydecreasedcellsurvival.TheseresultsdemonstratethatPM2.5exposurecaninducecytotoxicityandautophagyinHUVECsandthatautophagyplayaprotectiveroleagainstPM2.5-inducedcytotoxicity.ThefindingsofthepresentstudyimplyadirecttoxiceffectofPM2.5onHUVECsandprovidenovelinsightintothemechanismofcardiovasculardiseasescausedbyPM2.5exposure. ...
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