Extracorporeal cardiac shock waves therapy promotes function of endothelial progenitor cells through PI3K/AKT and MEK/ERK signaling pathways.
Extracorporeal cardiac shock waves therapy promotes function of endothelial progenitor cells through PI3K/AKT and MEK/ERK signaling pathways.
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体外心脏冲击波疗法通过 PI3K/AKT 和 MEK/ERK 信号通路促进内皮祖细胞的功能。
DOI：
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发表时间：
2020-07
影响因子：
2.2
通讯作者：
Cai Hongyan
中科院分区：
文献类型：
--
作者：
Ma Yiming;Hu Zhao;Yang Dan;Li Li;Wang Luqiao;Xiao Jianming;Cao Xingyu;Shi Yunke;Cai Hongyan
以往的研究表明，体外心脏冲击波(ECSW)作为一种安全、有效、非侵入性的血管生成方法，可以诱导冠心病患者的血管生成并改善其心功能。内皮祖细胞可以迁移到缺血心肌并分化为血管内皮细胞，从而促进血管生成。体外冲击波能否改善内皮祖细胞的血管生成能力尚不清楚。本课题研究体外冲击波治疗对内皮祖细胞功能及相关信号转导通路的影响。采用密度离心法分离SD大鼠骨髓内皮祖细胞。体外冲击波(500次/mm2，0.09mJ/mm2)处理后，内皮祖细胞的细胞活力、抗凋亡、迁移和管状形成均显著改善。此外，体外冲击波治疗后，磷酸化的AKT和ERK表达增加，下游信号分子eNOS和Bcl2表达增加，Bax和Caspase3表达降低。但PI3K/AKT抑制剂LY294002和MEK/ERK抑制剂PD98059可抑制上述有益作用。总之，ECSW可以通过PI3K/AKT和MEK/ERK信号通路促进EPC的存活、迁移和血管生成能力，抑制EPC的凋亡。其机制可能与通过PI3K/AKT和MEK/ERK信号通路促进下游p-eNOS和抗凋亡蛋白Bcl2的表达，抑制促凋亡蛋白Bax和Caspase3的表达有关。
Previous studies have demonstrated extracorporeal cardiac shock waves (ECSW) could induce angiogenesis and improves myocardial function in patients with coronary heart diseases as a safe, effective, and non-invasive angiogenic approach. The endothelial progenitor cells (EPCs) can migrate to the ischemic myocardium and differentiate into vascular endothelial cells, thus promoting the angiogenesis. Whether ECSW can improve the angiogenic ability of EPCs is unclear. This topic studied the effects of ECSW Therapy on EPCs functions and related signal transduction pathways. The bone marrow-derived EPCs of SD rats were isolated by the density centrifugation method. After treatment with ECSW (500 shots at 0.09 mJ/mm2), the cell viability, anti-apoptosis, migration, and tube formation of EPCs were significantly improved. In addition, the expressions of phosphorylated AKT and ERK were increased after ECSW treatment, the expressions of downstream signaling molecules eNOS and Bcl-2 were also increased, but the expressions of Bax and Caspase3 were decreased. However, these beneficial effects can be inhibited by PI3K/AKT inhibitor LY294002 and MEK/ERK inhibitor PD98059. Together, ECSW can promote the cell viability, migration, and angiogenic ability of EPCs and inhibit the apoptosis of EPCs through the PI3K/AKT and MEK/ERK signaling pathways. The mechanism may be related to promoting the expressions of downstream p-eNOS and anti-apoptotic protein Bcl-2 and inhibiting the expressions of pro-apoptotic protein Bax and Caspase3 through the PI3K/AKT and MEK/ERK signaling pathways.
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影响因子：
7.5
作者：
沈成兴
通讯作者：
沈成兴
DOI：
10.1152/ajpheart.00113.2006
发表时间：
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影响因子：
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作者：
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影响因子：
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影响因子：
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作者：
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影响因子：
4.5
作者：
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