作者: Eric A. Shikatani , Mark Chandy , Rickvinder Besla , Cedric C. Li , Abdul Momen
DOI: 10.1161/ATVBAHA.115.307116
关键词:
摘要: Objective—Vascular smooth muscle cells (VSMCs) are believed to dedifferentiate and proliferate in response vessel injury. Recently, adventitial progenitor were implicated as a source of VSMCs involved remodeling. c-Myb is transcription factor known regulate VSMC proliferation vivo differentiation from mouse embryonic stem cell–derived progenitors vitro. However, the role regulating specific adult vascular cell populations was not known. Our objective examine Sca1+ cells. Approach Results—Using mice with wild-type or hypomorphic c-myb (c-mybh/h), BrdU (bromodeoxyuridine) uptake flow cytometry revealed defective at 8, 14, 28 days post carotid artery denudation injury c-mybh/h arteries. cKit+CD34−Flk1−Sca1+CD45−Lin− failed proliferate, suggesting that re...