Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI 48201, USA.
Photochem Photobiol Sci. 2011 Apr;10(4):491-8. doi: 10.1039/c0pp00276c. Epub 2010 Dec 2.
In this report, we describe an effect of photodynamic therapy (PDT) on membrane trafficking in murine 1c1c7 hepatoma cells. A brief exposure of 1c1c7 cells to a 20 nM concentration of the phosphatidylinositol kinase class-3 antagonist wortmannin led to the rapid appearance of cytoplasmic vacuoles. Fluorescence monitoring of plasma membrane-associated 1-[4-(trimethylamino)phenyl]-6-phenylhexa-1,3,5-triene (TDPH) over time demonstrated that the wortmannin-induced vacuoles were derived from endocytosed plasma membrane. Low-dose photodamage catalyzed by the lysosomal photosensitizer NPe6, prior to the addition of wortmannin, prevented formation of these vacuoles. NPe6 was found to suppress for several hours the normal trafficking of TDPH-labeled plasma membrane to the cytosol, and the formation of punctate TDPH-labeled cytoplasmic vesicles. The ability of NPe6-induced photodamage to suppress wortmannin-induced vacuolization occurred under conditions that did not disrupt lysosomes and were at or below the threshold of cytostatic/cytotoxic effects. Furthermore, the suppressive effects of NPe6-PDT were not prevented by inclusion of an agent that stabilized lysosomal membranes, or by E64d, an inhibitor of lysosomal cathepsin proteases. Mitochondrial photodamage was less effective at preventing wortmannin-induced vacuole formation and PDT directed against the ER had no effect. The role of photodamage to the endocytic pathway may be a hitherto unexplored effect on cells that selectively accumulate photosensitizing agents. These results indicate that photodamage directed against endosomes/lysosomes has effects independent of the release of lysosomal proteases.
在本报告中,我们描述了光动力疗法 (PDT) 对鼠 1c1c7 肝癌细胞膜运输的影响。1c1c7 细胞短暂暴露于 20 nM 浓度的磷脂酰肌醇激酶 3 类拮抗剂wortmannin,会迅速出现细胞质空泡。随着时间的推移,对与质膜相关的 1-[4-(三甲基氨基)苯基]-6-苯基己-1,3,5-三烯 (TDPH) 的荧光监测表明,wortmannin 诱导的空泡来自内吞的质膜。在添加 wortmannin 之前,溶酶体光敏剂 NPe6 催化的低剂量光损伤会阻止这些空泡的形成。研究发现,NPe6 在数小时内抑制 TDPH 标记的质膜正常转运到细胞质,并形成点状 TDPH 标记的细胞质小泡。NPe6 诱导的光损伤抑制 wortmannin 诱导的空泡形成的能力发生在不破坏溶酶体的条件下,并且处于或低于细胞生长抑制/细胞毒性作用的阈值。此外,NPe6-PDT 的抑制作用不会被包含稳定溶酶体膜的试剂或溶酶体组织蛋白酶蛋白酶抑制剂 E64d 所阻止。线粒体光损伤在防止 wortmannin 诱导的空泡形成方面效果较差,而针对内质网的 PDT 则没有效果。光损伤对吞噬途径的作用可能是对选择性积累光敏剂的细胞的一种迄今尚未探索的影响。这些结果表明,针对内体/溶酶体的光损伤具有独立于溶酶体蛋白酶释放的作用。