0305国际期刊速递丨今日热点急性心

TODAY今日发布CATHETERCARDIOINTEEarlyRecent,Mar04,今日发布04篇NEJMMar05,:(10)今日发布21篇JAHAMar17,:9(6)今日发布03篇ATVBEarlyRecent,Mar05,今日发布04篇CirculationResearchEarlyRecent,Mar05,今日发布01篇RECOMMEND推荐阅读01内皮靶向性microRNA-15a/16-1缺失促进脑卒中后血管生成和改善长期神经功能恢复CirculationResearchresearch-articlePingSun,KaiZhang,etc.1小时前等79用户推荐阅读本文Rationale:Angiogenesispromotesneurologicalrecoveryafterstrokeandisassociatedwithlongersurvivalofstrokepatients.CerebralangiogenesisistightlycontrolledbycertainmicroRNAs(miRs),suchasthemiR-15a/16-1cluster,amongothers.However,thefunctionofthemiR-15a/16-1clusterinendotheliumonpost-ischemiccerebralangiogenesisisnotknown.血管生成促进脑卒中后神经功能的恢复，并与脑卒中患者的生存期延长有关。脑血管生成受到某些microRNAs（miR）的严格控制，如miR-15a/16-1簇等。然而，内皮细胞miR-15a/16-1簇在脑缺血后血管生成中的作用尚不清楚。Objective:ToinvestigatethefunctionalsignificanceandmolecularmechanismofendothelialmiR-15a/16-1clusteronangiogenesisintheischemicbrain.探讨内皮细胞miR-15a/16-1簇在缺血性脑血管生成中的作用及分子机制。MethodsandResults:Endothelialcell-selectivemiR-15a/16-1conditionalknockout(EC-miR-15a/16-1cKO)miceandWTlittermatecontrolsweresubjectedto1hmiddlecerebralarteryocclusion(MCAO)followedby28dreperfusion.DeletionofmiR-15a/16-1clusterinendotheliumattenuatespost-strokebraininfarctionandatrophy,andimprovesthelong-termsensorimotorandcognitiverecoveryagainstischemicstroke.Endothelium-targeteddeletionofthemiR-15a/16-1clusteralsoenhancespost-strokeangiogenesisbypromotingvascularremodelingandstimulatingthegenerationofnewlyformedfunctionalvessels,andincreasestheipsilateralcerebralbloodflow.Endothelialcell-selectivedeletionofthemiR-15a/16-1clusterup-regulatedtheproteinexpressionofpro-angiogenicfactorsvascularendothelialgrowthfactor(VEGFA),fibroblastgrowthfactor2(FGF2),andtheirreceptorsVEGFR2andFGFR1afterischemicstroke.Consistently,lentiviralknockdownofthemiR-15a/16-1clusterinprimarymouseorhumanbrainmicrovascularendothelialcellculturesenhancedinvitroangiogenesisandup-regulatedpro-angiogenicproteinsexpressionafteroxygen-glucosedeprivation(OGD),whereaslentiviraloverexpressionofthemiR-15a/16-1clustersuppressedinvitroangiogenesisanddown-regulatedpro-angiogenicproteinsexpression.Mechanistically,miR-15a/16-1translationallyrepressespro-angiogenicfactorsVEGFA,FGF2,andtheirreceptorsVEGFR2andFGFR1,respectively,bydirectlybindingtothe

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