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目的观察不同的剪切力对体外培养的大鼠肺微血管内皮细胞(PMVECs)细胞骨架蛋白(F-actin)的影响,探讨高血流性肺动脉高压的早期发病机制。方法用自制的多层流动腔对体外培养的大鼠PMVECs施加剪切力作用,以异硫氰酸荧光素-毒蕈肽标记F-actin,采用共聚焦显微镜扫描观察F-actin的变化并记录相应的荧光值。结果剪切力引起PMVECs骨架内的微丝重排,向着剪切力的方向出现与细胞长轴一致的应力纤维,且剪切力越大、作用时间越长,这种现象越明显,直至细胞内几乎所有的微丝F-actin都沿着细胞长轴形成应力纤维。结论PMVECs细胞骨架在受到剪切力作用后会形成应力纤维,该现象在剪切力作用早期即可发生,并且对作用时间及剪切力大小具有依赖性,这可能与高血流性肺动脉高压的早期发病机制密切相关。
Objective To observe the effects of different shear forces on the cytoskeleton protein (F-actin) in cultured rat pulmonary microvascular endothelial cells (PMVECs) in vitro and to explore the early pathogenesis of hypertensive pulmonary hypertension. Methods A self-made multi-layer flow chamber was used to exert shear force on cultured rat PMVECs. F-actin was labeled with fluorescein isothiocyanate-toxin and the change of F-actin was observed by confocal microscopy The corresponding fluorescence value. Results Shear force caused the rearrangement of actin filaments in the framework of PMVECs. The stress fibers appeared consistent with the long axis of the cells in the direction of shearing force. The larger the shearing force and the longer the acting time, the more obvious the phenomenon was until the cells Almost all microfilament F-actin forms stress fibers along the long axis of the cell. Conclusions The cytoskeleton of PMVECs will form stress fibers after being subjected to shear stress. This phenomenon may occur in the early stage of shear stress and is dependent on the duration of action and the magnitude of shear force, which may be related to high blood flow pulmonary hypertension The early pathogenesis is closely related.