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Responses of of adventitial CD34(+) vascular wall-resident stem/progenitor cells and medial smooth muscle cells to carotid injury in rats

机译:外膜CD34(+)血管壁驻留干/祖细胞和内侧平滑肌细胞对大鼠颈动脉损伤的反应

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Cell culture and carotid injury studies with SD rats were performed to investigate the roles of CD34(+) vascular wall-resident stem/progenitor cells (VRS/Pcs) and vascular smooth muscle cells (SMCs) in neointimal formation. In vitro, the media-isolated SM MHC+ SMCs occupied 93.92 +/- 8.62% of total BrdU(+) cells, whereas the CD34(+) cells, only 2.61 +/- 0.82%, indicating that the cell expansion in SMC culture was attributed to SM MHC+ SMCs. The adventitia-isolated CD34(+) VRS/Pcs responded to PDGF-BB by differentiating into SMC-like cells which expressed SM22 alpha (an early stage SMC marker), but seldom SM MHC (a late stage SMC marker). In carotid injury model, the CD34(+) VRS/Pcs differentiated SMC-like cells migrated in very few numbers into only the outer layer of the media, and this was further confirmed by a cell tracking analysis. While the neointimal cells were consistently SM MHC+ and CD34(-) SMCs during whole course of the post-injury remodeling. Thus it is speculated that the adventitial CD34(+) VRS/Pcs, at least in rat model, do not directly participate in neointimal formation, but function to maintain homeostasis of the media during injury-induced vascular wall remodeling. (C) 2016 Elsevier Inc. All rights reserved.
机译:进行了SD大鼠细胞培养和颈动脉损伤研究,以研究CD34(+)血管壁驻留干/祖细胞(VRS / Pcs)和血管平滑肌细胞(SMCs)在新内膜形成中的作用。在体外,培养基分离的SM MHC + SMC占总BrdU(+)细胞的93.92 +/- 8.62%,而CD34(+)细胞仅占2.61 +/- 0.82%,表明SMC培养中的细胞扩增是归因于SM MHC + SMC。外膜分离的CD34(+)VRS / Pcs通过分化成表达SM22 alpha(早期SMC标记)但很少表达SM MHC(晚期SMC标记)的SMC样细胞来响应PDGF-BB。在颈动脉损伤模型中,CD34(+)VRS / Pcs分化的SMC样细胞仅以极少数的数量迁移到培养基的外层,并且通过细胞追踪分析进一步证实了这一点。尽管新内膜细胞在损伤后重塑的整个过程中始终是SM MHC +和CD34(-)SMC。因此推测,至少在大鼠模型中,外膜CD34(+)VRS / Pcs不直接参与新内膜形成,而是在损伤诱导的血管壁重塑过程中维持培养基的稳态。 (C)2016 Elsevier Inc.保留所有权利。

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