Tokyo University of Pharmacy and Life Sciences, 1432-1 Horinouchi, Hachioji, Tokyo 192-0392, Japan.
FEBS Lett. 2010 Mar 5;584(5):1016-20. doi: 10.1016/j.febslet.2010.01.055. Epub 2010 Jan 31.
We have recently demonstrated that reactive oxygen species (ROS) play an important role in RAW264.7 cell apoptosis induced by cationic liposomes composed of stearylamine (SA-liposomes). In this study, we investigated whether protein kinase Cdelta PKCdelta) is involved in apoptosis induced by cationic liposomes. Tyrosine phosphorylation, nuclear localization, and cleavage of PKCdelta were observed following the treatment of cells with SA-liposomes, suggesting that SA-liposomes activate PKCdelta. Rottlerin, a specific inhibitor of PKCdelta, inhibited ROS generation and also suppressed apoptosis. Cell surface proteoglycans may contribute to PKCdelta activation by SA-liposomes. These findings suggest that PKCdelta is strongly associated with apoptosis induced by SA-liposomes.
我们最近的研究表明，活性氧（ROS）在由硬脂胺（SA）组成的阳离子脂质体诱导 RAW264.7 细胞凋亡中发挥重要作用。在本研究中，我们探讨了蛋白激酶 C 亚型 δ（PKCδ）是否参与阳离子脂质体诱导的细胞凋亡。用 SA 脂质体处理细胞后，观察到 PKCδ的酪氨酸磷酸化、核定位和裂解，提示 SA 脂质体激活了 PKCδ。PKCδ的特异性抑制剂罗特林（rottlerin）抑制 ROS 的产生，同时也抑制细胞凋亡。细胞表面糖蛋白可能通过 SA 脂质体促进 PKCδ的激活。这些发现表明，PKCδ与 SA 脂质体诱导的细胞凋亡密切相关。
