SUMO2/3 缀合是一种内源性神经保护机制。
SUMO2/3 conjugation is an endogenous neuroprotective mechanism.
机构信息
Center for Stroke Research Berlin, Department of Experimental Neurology, Charité Universitätsmedizin Berlin, Berlin, Germany.
出版信息
J Cereb Blood Flow Metab. 2011 Nov;31(11):2152-9. doi: 10.1038/jcbfm.2011.112. Epub 2011 Aug 24.
Abstract
Small ubiquitin-like modifier (SUMO)2/3 but not SUMO1 conjugation is activated after transient cerebral ischemia. To investigate its function, we blocked neuronal SUMO2/3 translation through lentiviral microRNA delivery in primary cortical neurons. Viability was unaffected by SUMO2/3 silencing unless neurons were stressed by transient oxygen-glucose deprivation (OGD). Both 15 and 45 minutes of OGD were tolerated by control microRNA-expressing neurons but damaged >60% of neurons expressing SUMO2/3 microRNA. Damaging OGD (75 minutes) increased neuronal loss to 54% (control microRNA) and to 99% (SUMO2/3 microRNA). This suggests that activation of SUMO2/3 conjugation is an endogenous neuroprotective stress response.
摘要
小泛素样修饰物 (SUMO)2/3 但不是 SUMO1 缀合在短暂性脑缺血后被激活。为了研究其功能，我们通过慢病毒 microRNA 传递在原代皮质神经元中阻断神经元 SUMO2/3 翻译。SUMO2/3 沉默对神经元活力没有影响，除非神经元受到短暂性氧葡萄糖剥夺 (OGD) 的应激。对照 microRNA 表达神经元耐受 15 和 45 分钟的 OGD，但表达 SUMO2/3 microRNA 的神经元损伤超过 60%。损伤性 OGD（75 分钟）导致神经元丢失增加到 54%（对照 microRNA）和 99%（SUMO2/3 microRNA）。这表明 SUMO2/3 缀合的激活是一种内源性的神经保护应激反应。
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