From the Department of Systems Biology, Yonsei University College of Life Science and Biotechnology, Seoul 120-749, Korea.
J Biol Chem. 2013 Dec 20;288(51):36717-32. doi: 10.1074/jbc.M113.492876. Epub 2013 Nov 14.
Calpains are a family of calcium-dependent cysteine proteases that are ubiquitously expressed in mammals and play critical roles in neuronal death by catalyzing substrate proteolysis. Here, we developed two-dimensional gel electrophoresis-based protease proteomics to identify putative calpain substrates. To accomplish this, cellular lysates from neuronal cells were first separated by pI, and the immobilized sample on a gel strip was incubated with a recombinant calpain and separated by molecular weight. Among 25 altered protein spots that were differentially expressed by at least 2-fold, we confirmed that arsenical pump-driving ATPase, optineurin, and peripherin were cleaved by calpain using in vitro and in vivo cleavage assays. Furthermore, we found that all of these substrates were cleaved in MN9D cells treated with either ionomycin or 1-methyl-4-phenylpyridinium, both of which cause a calcium-mediated calpain activation. Their cleavage was blocked by calcium chelator or calpain inhibitors. In addition, calpain-mediated cleavage of these substrates and its inhibition by calpeptin were confirmed in a middle cerebral artery occlusion model of cerebral ischemia, as well as a stereotaxic brain injection model of Parkinson disease. Transient overexpression of each protein was shown to attenuate 1-methyl-4-phenylpyridinium-induced cell death, indicating that these substrates may confer protection of varying magnitudes against dopaminergic injury. Taken together, the data indicate that our protease proteomic method has the potential to be applicable for identifying proteolytic substrates affected by diverse proteases. Moreover, the results described here will help us decipher the molecular mechanisms underlying the progression of neurodegenerative disorders where protease activation is critically involved.
钙蛋白酶是一类依赖于钙离子的半胱氨酸蛋白酶,广泛存在于哺乳动物中,通过催化底物蛋白水解,在神经元死亡中发挥关键作用。在这里,我们开发了基于二维凝胶电泳的蛋白酶组学方法来鉴定潜在的钙蛋白酶底物。为了实现这一目标,首先将神经元细胞的细胞裂解物通过等电点分离,然后将固定在凝胶条上的样品与重组钙蛋白酶孵育,并通过分子量进行分离。在至少 2 倍差异表达的 25 个改变的蛋白质斑点中,我们通过体外和体内切割实验证实砷泵驱动的 ATP 酶、optineurin 和 peripherin 被钙蛋白酶切割。此外,我们发现所有这些底物在离子霉素或 1-甲基-4-苯基吡啶处理的 MN9D 细胞中均被切割,这两种物质均可导致钙介导的钙蛋白酶激活。它们的切割被钙螯合剂或钙蛋白酶抑制剂阻断。此外,在大脑中动脉闭塞模型的脑缺血和帕金森病的立体定向脑内注射模型中,也证实了钙蛋白酶对这些底物的切割及其对 calpeptin 的抑制作用。瞬时过表达每种蛋白均能减轻 1-甲基-4-苯基吡啶诱导的细胞死亡,表明这些底物可能对多巴胺能损伤具有不同程度的保护作用。综上所述,数据表明我们的蛋白酶组学方法有可能适用于鉴定受多种蛋白酶影响的水解底物。此外,这里描述的结果将有助于我们破译蛋白酶激活至关重要的神经退行性疾病进展的分子机制。