Baek Suji, Lee Kang Pa, Cui Long, Ryu Yunkyoung, Hong Jung Min, Kim Junghwan, Jung Seung Hyo, Bae Young Min, Won Kyung Jong, Kim Bokyung
Department of Physiology, School of Medicine, Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul, 05029, South Korea.
Department of Physical Therapy, College of Public Health & Welfare, Yongin University, Yongin, 17092, South Korea.
Lasers Med Sci. 2017 Dec;32(9):2121-2127. doi: 10.1007/s10103-017-2338-z. Epub 2017 Oct 5.
Vascular restenosis after injury of blood vessel has been implicated in various responses including apoptosis, migration, and proliferation in vascular smooth muscle cells (VSMCs) stimulated by diverse growth factors underlying platelet-derived growth factor (PDGF). Previous studies evaluated the effects of low-power laser (LPL) irradiation over various wavelength ranges on VSMC events in normal and pathologic states. However, whether VSMC responses are affected by LPL irradiation remains unclear. The purpose of this study is to explore the effects of LPL (green diode laser 532-nm pulsed wave of 300 mW at a spot diameter of 1 mm) irradiation on the responses, apoptosis, migration, and proliferation of VSMCs. The effect of LPL irradiation was tested on VSMCs through cytotoxicity, proliferation, migration, and apoptotic assays. Aortic ring assay was used to assess the effect of LPL irradiation on aortic sprout outgrowth. Protein expression levels were determined by western blotting. LPL irradiation did not affect VSMC viability but slightly attenuated PDGF-BB-induced proliferation in VSMCs. In addition, LPL irradiation inhibited PDGF-BB-evoked migration of VSMCs. Aortic sprout outgrowth in response to PDGF-BB was diminished in cells treated with LPL. In contrast, LPL irradiation evoked apoptosis in VSMCs in the presence of PDGF-BB. Similarly, activation of caspase-3 and Bax, as well as p38 mitogen-activated protein kinase (MAPK), in VSMCs treated with PDGF-BB was enhanced by exposure to LPL. These findings indicate that LPL irradiation induces vascular apoptosis via p38 MAPK activation and simultaneously inhibits VSMC proliferation and migration in response to PDGF-BB.
血管损伤后的血管再狭窄与多种反应有关,包括血小板衍生生长因子(PDGF)等多种生长因子刺激下血管平滑肌细胞(VSMCs)的凋亡、迁移和增殖。先前的研究评估了不同波长范围内的低功率激光(LPL)照射对正常和病理状态下VSMC事件的影响。然而,LPL照射是否会影响VSMC反应仍不清楚。本研究的目的是探讨LPL(波长532 nm、光斑直径1 mm、功率300 mW的绿色二极管激光脉冲波)照射对VSMCs反应、凋亡、迁移和增殖的影响。通过细胞毒性、增殖、迁移和凋亡试验检测LPL照射对VSMCs的影响。采用主动脉环试验评估LPL照射对主动脉芽生长的影响。通过蛋白质印迹法测定蛋白质表达水平。LPL照射不影响VSMC活力,但略微减弱了PDGF-BB诱导的VSMCs增殖。此外,LPL照射抑制了PDGF-BB引起的VSMCs迁移。在用LPL处理的细胞中,对PDGF-BB的主动脉芽生长减少。相反,在存在PDGF-BB的情况下,LPL照射可诱导VSMCs凋亡。同样,暴露于LPL可增强PDGF-BB处理的VSMCs中caspase-3和Bax以及p38丝裂原活化蛋白激酶(MAPK)的激活。这些发现表明,LPL照射通过激活p38 MAPK诱导血管凋亡,同时抑制VSMCs对PDGF-BB的增殖和迁移反应。