溶酶体
光动力疗法
细胞凋亡
细胞生物学
光敏剂
内质网
线粒体
化学
程序性细胞死亡
生物
生物化学
酶
有机化学
作者
Song‐mao Chiu,Liang‐yan Xue,Minh Lam,Myriam E. Rodríguez,Ping Zhang,Malcolm E. Kenney,Anna‐Liisa Nieminen,Nancy L. Oleinick
标识
DOI:10.1111/j.1751-1097.2010.00766.x
摘要
Abstract Photodynamic therapy (PDT) with lysosome‐targeted photosensitizers induces the intrinsic pathway of apoptosis via the cleavage and activation of the BH3‐only protein Bid by proteolytic enzymes released from photodisrupted lysosomes. To investigate the role of Bid in apoptosis induction and the role of damaged lysosomes on cell killing by lysosome‐targeted PDT, we compared the responses of wild type and Bid‐knock‐out murine embryonic fibroblasts toward a mitochondrion/endoplasmic reticulum‐binding photosensitizer, Pc 4, and a lysosome‐targeted sensitizer, Pc 181. Whereas apoptosis and overall cell killing were induced equally well by Pc 4‐PDT in both cell lines, Bid −/− cells were relatively resistant to induction of apoptosis and to overall killing following PDT with Pc 181, particularly at low PDT doses. Thus, Bid is critical for the induction of apoptosis caused by PDT with the lysosome‐specific sensitizers, but dispensable for PDT targeted to other membranes.
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