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dc.contributor.authorTang, Juan
dc.contributor.authorWang, Haixiao
dc.contributor.authorHuang, Xiuzhen
dc.contributor.authorLi, Fei
dc.contributor.authorZhu, Huan
dc.contributor.authorLi, Yan
dc.contributor.authorHe, Lingjuan
dc.contributor.authorZhang, Hui
dc.contributor.authorPu, Wenjuan
dc.contributor.authorLiu, Kuo
dc.contributor.authorZhao, Huan
dc.contributor.authorBentzon, Jacob F 
dc.contributor.authorYu, Ying
dc.contributor.authorJi, Yong
dc.contributor.authorNie, Yu
dc.contributor.authorTian, Xueying
dc.contributor.authorZhang, Li
dc.contributor.authorGao, Dong
dc.contributor.authorZhou, Bin
dc.identifier.citationCell Stem Cell. 2020; 26(1):81-96 e4es_ES
dc.description.abstractRapid regeneration of smooth muscle after vascular injury is essential for maintaining arterial function. The existence and putative roles of resident vascular stem cells (VSCs) in artery repair are controversial, and vessel regeneration is thought to be mediated by proliferative expansion of pre-existing smooth muscle cells (SMCs). Here, we performed cell fate mapping and single-cell RNA sequencing to identify Sca1+ VSCs in the adventitial layer of artery walls. After severe injury, Sca1+ VSCs migrate into the medial layer and generate de novo SMCs, which subsequently expand more efficiently compared with pre-existing smooth muscle. Genetic lineage tracing using dual recombinases distinguished a Sca1+PDGFRa+ VSC subpopulation that generates SMCs, and genetic ablation of Sca1+ VSCs or specific knockout of Yap1 in Sca1+ VSCs significantly impaired artery repair. These findings provide genetic evidence of a bona fide Sca1+ VSC population that produces SMCs and delineates their critical role in vessel repair.es_ES
dc.description.sponsorshipWe thank Shanghai Model Organisms Center, Inc. (SMOC) for mouse generation, Dr. Camargo Fernando for Yap-flox mouse, and Baojin Wu, Guoyuan Chen, Zhonghui Weng, and Aimin Huang for animal husbandry. We also thank Wei Bian, Lin Qiu, and members of National Center for Protein Science Shanghai for technical help and assistance with microscopy. This work was supported by the Strategic Priority Research Program of the Chinese Academy of Sciences (CAS; XDA16010507 and XDB19000000), the National Key Research and Development Program of China (2019YFA0110400, 2018YFA0107900, 2018YFA0108100, 2016YFC1300600, and 2017YFC1001303), the Shanghai Zhangjiang Stem Cell Project (ZJ2018-ZD-004), the National Science Foundation of China (31730112, 91639302, 31625019, 91849202, 81761138040, 81872241, 31701292, 31801215, and 31922032), the Youth Innovation Promotion Association of the CAS, the Key Project of Frontier Sciences of the CAS (QYZDB-SSW-SMC003), the Shanghai Science and Technology Commission (19JC1415700, 17ZR1449600, and 17ZR1449800), the Program for Guangdong Introduction Innovative and Entrepreneurial Teams (2017ZT07S347), the Major Program of the Development Fund for the Shanghai Zhangjiang National Innovation Demonstration Zone (Stem Cell Strategic Biobank and Stem Cell Clinical Technology Transformation Platform, ZJ2018-ZD-004), the Shanghai Yangfan Project, the China Postdoctoral Science Foundation, the China Postdoctoral Innovative Talent Support Program, the Young Elite Scientist Sponsorship Program by CAST (2018QNRC001, and 2017QNRC001), Boehringer Ingelheim, a Sanofi-SIBS fellowship, AstraZeneca, and a Royal Society Newton advanced fellowship.es_ES
dc.publisherCell Press es_ES
dc.subjectDual recombinasees_ES
dc.subjectGenetic lineagees_ES
dc.subjectVascular stem celles_ES
dc.subjectVessel injuryes_ES
dc.titleArterial Sca1+ Vascular Stem Cells Generate De Novo Smooth Muscle for Artery Repair and Regenerationes_ES
dc.typejournal articlees_ES
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.identifier.journalCell stem celles_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Patología Experimental de la Aterosclerosises_ES
dc.rights.accessRightsembargoed accesses_ES

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Attribution-NonCommercial-NoDerivatives 4.0 Internacional
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