Migration versus proliferation as contributor to in vitro wound healing of vascular endothelial and smooth muscle cells
Migration versus proliferation as contributor to in vitro wound healing of vascular endothelial and smooth muscle cells
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DOI：
10.1016/j.yexcr.2019.01.011
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发表时间：
2019-03-01
影响因子：
3.7
通讯作者：
Slepian, Marvin J.
中科院分区：
文献类型：
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作者：
Ammann, Kaitlyn R.;DeCook, Katrina J.;Slepian, Marvin J.
作为细胞集体生长的结果，伤口愈合是对损伤的基本生物学反应。在血管生物学领域，血管平滑肌细胞（SMCs）和内皮细胞（ECs）对损伤和底物表面的反应在血管成形术和动脉粥样硬化切除术等治疗性临床治疗干预措施中具有重要意义。具体来说，细胞在损伤刺激下闭合伤口（即增殖与迁移）的机制对更好地调节复发性血管狭窄、预防血栓形成、闭塞和危及生命的心血管事件具有重要意义。在这里，我们研究了伤口或间隙引入血管间充质干细胞或内皮细胞融合单层后的生长程度和时间顺序。观察到这些细胞关闭伤口或间隙的首选机制存在显着差异；48 h后，73%的SMC创口闭合是由于增殖引起的，而75%的EC创口闭合是由于迁移引起的。这些机制可以通过添加或去除细胞外基质基质和损伤来进一步调节，与SMCs相比，ECs对基质成分的反应更强，对损伤的反应更小。我们的研究结果表明，ECs和SMCs愈合伤口的方式不同，损伤的时间和方式以及相关的底物表面都会影响这种反应。
Wound closure, as a result of collective cell growth, is an essential biological response to injury. In the field of vascular biology, the response of vascular smooth muscle cells (SMCs) and endothelial cells (ECs) to injury and substrate surface is important in therapeutic clinical treatment interventions such as angioplasty and atherectomy. Specifically, the mechanism by which cells close wounds (i.e. proliferation versus migration) in response to injury stimuli is of interest to better modulate recurrent vascular stenosis, prevent thrombus formation, occlusion, and life-threatening cardiovascular events. Here, we examine growth extent and temporal sequence of events following wound or gap introduction to a confluent monolayer of vascular SMCs or ECs. Significant differences in the preferred mechanisms of these cells to close wounds or gaps were observed; after 48 h, 73% of SMC wound closure was observed to be due to proliferation, while 75% of EC wound closure resulted from migration. These mechanisms were further modulated via addition or removal of extracellular matrix substrate and injury, with ECs more responsive to substrate composition and less to injury, in comparison to SMCs. Our results indicate that ECs and SMCs heal wounds differently, and that the time and mode of injury and associated substrate surface all impact this response.