MRC Centre for Synaptic Plasticity, School of Biochemistry, University of Bristol, University Walk, Bristol, UK.
J Cereb Blood Flow Metab. 2012 Jan;32(1):17-22. doi: 10.1038/jcbfm.2011.146. Epub 2011 Oct 12.
Here, we show that oxygen and glucose deprivation (OGD) causes increased small ubiquitin-like modifier (SUMO)-1 and SUMO-2/3 conjugation to substrate proteins in cultured hippocampal neurones. Surprisingly, the SUMO protease SENP-1, which removes SUMO from conjugated proteins, was also increased by OGD, suggesting that the neuronal response to OGD involves a complex interplay between SUMOylation and deSUMOylation. Importantly, decreasing global SUMOylation in cultured hippocampal neurones by overexpression of the catalytic domain of SENP-1 increased neuronal vulnerability to OGD-induced cell death. Taken together, these results suggest a neuroprotective role for neuronal SUMOylation after OGD.
在这里，我们表明，缺氧和葡萄糖剥夺（OGD）会导致培养的海马神经元中底物蛋白的小泛素样修饰物（SUMO）-1 和 SUMO-2/3 缀合增加。令人惊讶的是，SUMO 蛋白酶 SENP-1 也被 OGD 增加，这表明神经元对 OGD 的反应涉及 SUMO 化和去 SUMO 化之间的复杂相互作用。重要的是，通过过表达 SENP-1 的催化结构域，在培养的海马神经元中降低全局 SUMO 化，会增加神经元对 OGD 诱导的细胞死亡的易感性。总之，这些结果表明神经元 SUMO 化在 OGD 后具有神经保护作用。
