Department of Ecology, Faculty of Mathematical, Physical and Natural Sciences (SMFN), University of Calabria, Cosenza, Italy.
Oxid Med Cell Longev. 2011;2011:282739. doi: 10.1155/2011/282739. Epub 2011 Sep 13.
The word autophagy broadly refers to the cellular catabolic processes that lead to the removal of damaged cytosolic proteins or cell organelles through lysosomes. Although autophagy is often observed during programmed cell death, it may also serve as a cell survival mechanism. Accumulation of reactive oxygen species within tissues and cells induces various defense mechanisms or programmed cell death. It has been shown that, besides inducing apoptosis, oxidative stress can also induce autophagy. To date, however, the regulation of autophagy in response to oxidative stress remains largely elusive and poorly understood. Therefore, the present study was designed to examine the ratio between oxidative stress and autophagy in macrophages after oxidant exposure (AAPH) and to investigate the ultrastructural localization of beclin-1, a protein essential for autophagy, under basal and stressful conditions. Our data provide evidence that oxidative stress induces autophagy in macrophages. We demonstrate, for the first time by immunoelectron microscopy, the subcellular localization of beclin-1 in autophagic cells.
自噬一词广义上是指导致通过溶酶体去除受损的细胞质蛋白或细胞细胞器的细胞分解代谢过程。虽然自噬通常在程序性细胞死亡期间观察到，但它也可以作为一种细胞存活机制。组织和细胞内活性氧物质的积累会诱导各种防御机制或程序性细胞死亡。已经表明，除了诱导细胞凋亡外，氧化应激还可以诱导自噬。然而，迄今为止，氧化应激对自噬的调节在很大程度上仍难以捉摸且了解甚少。因此，本研究旨在研究氧化剂暴露（AAPH）后巨噬细胞中氧化应激与自噬之间的比率，并研究在基础和应激条件下自噬所必需的蛋白 beclin-1 的超微结构定位。我们的数据提供了氧化应激诱导巨噬细胞自噬的证据。我们首次通过免疫电镜证明了 beclin-1 在自噬细胞中的亚细胞定位。
