Delalande Anthony, Leduc Chloé, Midoux Patrick, Postema Michiel, Pichon Chantal
Centre de Biophysique Moléculaire, CNRS UPR4301, Orléans, France.
Centre de Biophysique Moléculaire, CNRS UPR4301, Orléans, France.
Ultrasound Med Biol. 2015 Jul;41(7):1913-26. doi: 10.1016/j.ultrasmedbio.2015.03.010. Epub 2015 Apr 27.
Microbubble oscillation at specific ultrasound settings leads to permeabilization of surrounding cells. This phenomenon, referred to as sonoporation, allows for the in vitro and in vivo delivery of extracellular molecules, including plasmid DNA. To date, the biological and physical mechanisms underlying this phenomenon are not fully understood. The aim of this study was to investigate the interactions between microbubbles and cells, as well as the intracellular routing of plasmid DNA and microbubbles, during and after sonoporation. High-speed imaging and fluorescence confocal microscopy of HeLa cells stably expressing enhanced green fluorescent protein fused with markers of cellular compartments were used for this investigation. Soft-shelled microbubbles were observed to enter cells during sonoporation using experimental parameters that led to optimal gene transfer. They interacted with the plasma membrane in a specific area stained with fluorescent cholera subunit B, a marker of lipid rafts. This process was not observed with hard-shelled microbubbles, which were not efficient in gene delivery under our conditions. The plasmid DNA was delivered to late endosomes after 3 h post-sonoporation, and a few were found in the nucleus after 6 h. Gene transfer efficacy was greatly inhibited when cells were treated with chlorpromazine, an inhibitor of the clathrin-dependent endocytosis pathway. In contrast, no significant alteration was observed when cells were treated with filipin III or genistein, both inhibitors of the caveolin-dependent pathway. This study emphasizes that microbubble-cell interactions do not occur randomly during sonoporation; microbubble penetration inside cells affects the efficacy of gene transfer at specific ultrasound settings; and plasmid DNA uptake is an active mechanism that involves the clathrin-dependent pathway.
在特定超声设置下微泡振荡会导致周围细胞的通透性增加。这种现象被称为声孔效应,它允许细胞外分子(包括质粒DNA)在体外和体内进行递送。迄今为止,这一现象背后的生物学和物理机制尚未完全明了。本研究的目的是调查声孔效应过程中及之后微泡与细胞之间的相互作用,以及质粒DNA和微泡在细胞内的转运途径。本研究使用高速成像和荧光共聚焦显微镜观察稳定表达与细胞区室标记物融合的增强型绿色荧光蛋白的HeLa细胞。使用导致最佳基因转移的实验参数,观察到软壳微泡在声孔效应过程中进入细胞。它们在荧光霍乱毒素B亚基染色的特定区域与质膜相互作用,荧光霍乱毒素B亚基是脂筏的标记物。在我们的条件下,硬壳微泡在基因递送方面效率不高,未观察到这种过程。声孔效应后3小时,质粒DNA被递送至晚期内体,6小时后在细胞核中发现少量质粒DNA。用氯丙嗪(一种网格蛋白依赖性内吞途径抑制剂)处理细胞时,基因转移效率受到极大抑制。相比之下,用菲律宾菌素III或染料木黄酮(两者均为小窝蛋白依赖性途径抑制剂)处理细胞时,未观察到明显变化。本研究强调,在声孔效应过程中,微泡与细胞之间的相互作用并非随机发生;微泡进入细胞内部会影响特定超声设置下的基因转移效率;并且质粒DNA的摄取是一种涉及网格蛋白依赖性途径的主动机制。