Low-level laser irradiation at a high power intensity increased human endothelial cell exosome secretion via Wnt signaling
Low-level laser irradiation at a high power intensity increased human endothelial cell exosome secretion via Wnt signaling
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DOI：
10.1007/s10103-018-2495-8
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发表时间：
2018-07-01
影响因子：
2.1
通讯作者：
Sokullu, Emel
中科院分区：
文献类型：
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作者：
Bagheri, Hesam Saghaei;Mousavi, Monireh;Sokullu, Emel
低强度激光照射(LLLI)对内皮细胞外切体生物发生的影响尚不清楚。我们推测，高剂量激光照射人内皮细胞可能通过Wnt信号通路参与调控外切体的生物发生。当LLLI的功率密度为80J/cm(2)时，人内皮细胞的存活率下降。通过表达CD63、Alix、Rab27a和b基因，照射后细胞释放外切体的能力显著增加。这与照射后24小时乙酰胆碱酯酶活性增强、伪足形成和Zeta电位值降低相一致。Western blotting显示Lc3的诱导和p62水平的降低，证实了自噬反应。流式细胞仪和电子显微镜分析显示，正常的Delta I活性表明线粒体功能处于健康状态，而PINK1和Optineurin的转录水平没有任何变化。高功率激光照射细胞后，p-Akt/Akt比值和体外小管生成能力减弱。PCR芯片和生物信息学分析表明，转录因子的诱导促进了Wnt信号通路和GTPase的活性。因此，在高功率强度下，LLLI通过诱导自噬和Wnt信号来增加外切体的生物发生。在高功率强度下，LLLI通过参与与Wnt信号和自噬刺激相关的转录因子来促进外切体的生物发生。
The distinct role of low-level laser irradiation (LLLI) on endothelial exosome biogenesis remains unclear. We hypothesize that laser irradiation of high dose in human endothelial cells (ECs) contributes to the modulation of exosome biogenesis via Wnt signaling pathway. When human ECs were treated with LLLI at a power density of 80 J/cm(2), the survival rate reduced. The potential of irradiated cells to release exosomes was increased significantly by expressing genes CD63, Alix, Rab27a, and b. This occurrence coincided with an enhanced acetylcholine esterase activity, pseudopodia formation, and reduced zeta potential value 24 h post-irradiation. Western blotting showed the induction of LC3 and reduced level of P62, confirming autophagy response. Flow cytometry and electron microscopy analyses revealed the health status of the mitochondrial function indicated by normal Delta I activity without any changes in the transcription level of PINK1 and Optineurin. When cells exposed to high power laser irradiation, p-Akt/Akt ratio and in vitro tubulogenesis capacity were blunted. PCR array and bioinformatics analyses showed the induction of transcription factors promoting Wnt signaling pathways and GTPase activity. Thus, LLLI at high power intensity increased exosome biogenesis by the induction of autophagy and Wnt signaling. LLLI at high power intensity increases exosome biogenesis by engaging the transcription factors related to Wnt signaling and autophagy stimulate.