Institute of Neuroscience, State Key Laboratory of Chemo/Biosensing and Chemometrics, College of Biology, Hunan University, Changsha, Hunan, 410082, China.
Department of Neurology, First Affiliated Hospital of Hunan University of Chinese Medicine, Changsha, Hunan, 410007, China.
Neurosci Lett. 2021 Mar 16;747:135662. doi: 10.1016/j.neulet.2021.135662. Epub 2021 Jan 20.
Stroke is one of the leading causes of death in adults worldwide. However, the mechanism causing neuronal death remains poorly understood. Our previous report showed that enolase1 (ENO1), a key glycolytic enzyme, alleviates cerebral ischemia-induced neuronal injury. It remained unclear whether enolase2 (ENO2) affects neuronal injury in stroke models. Here, we examined the effects of ENO2 in several stroke models. The results showed that the expression level of ENO2 was downregulated after 3 h of cerebral ischemia by middle cerebral artery occlusion (MCAO) in the mouse model. ENO2 was expressed in mouse brain and cultured hippocampus neurons. Overexpression of ENO2 in cultured hippocampus neurons did not affect neuronal injury in our oxygen-glucose deprivation (OGD) model. Interestingly, double knock-down (KD) of ENO1 and ENO2 increased neuronal injury while either KD of ENO1 or ENO2 failed to increase neuronal injury in OGD. Deletion of ENO1 did not affect anoxia-starvation (AS)-induced worm death in C. elegans. These findings demonstrated that ENO2 and ENO1 work together against neuronal injury in these stroke models.
中风是全球成年人死亡的主要原因之一。然而，导致神经元死亡的机制仍不清楚。我们之前的报告表明，烯醇化酶 1（ENO1）是一种关键的糖酵解酶，可减轻脑缺血引起的神经元损伤。ENO2 是否影响中风模型中的神经元损伤尚不清楚。在这里，我们研究了 ENO2 在几种中风模型中的作用。结果表明，在小鼠模型中，大脑中动脉闭塞（MCAO）导致的 3 小时脑缺血后 ENO2 的表达水平下调。ENO2 在小鼠大脑和培养的海马神经元中表达。在我们的氧葡萄糖剥夺（OGD）模型中，过表达 ENO2 不会影响神经元损伤。有趣的是，ENO1 和 ENO2 的双重敲低（KD）增加了神经元损伤，而 ENO1 或 ENO2 的 KD 均未能增加 OGD 中的神经元损伤。ENO1 的缺失不影响秀丽隐杆线虫中缺氧饥饿（AS）诱导的蠕虫死亡。这些发现表明，ENO2 和 ENO1 在这些中风模型中共同对抗神经元损伤。
