Ke Kaifu, Rui Ying, Li Lei, Zheng Heyi, Xu Wei, Tan Xiang, Cao Jianhua, Wu Xiaoyan, Cui Gang, Cao Maohong
Department of Neurology, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province, 226001, People's Republic of China.
J Mol Neurosci. 2014;54(2):171-80. doi: 10.1007/s12031-014-0271-1. Epub 2014 Mar 25.
EHD2, a member of the Eps15 homology domain (EH domain) family, is important for protein interactions during vesicular trafficking. Previous studies have proved that EHD2 can regulate trafficking from the plasma membrane in the process of endocytosis. However, its function in central nervous system diseases is still with limited understanding. In this frame, we found that EHD2 expression was upregulated in the perihematomal caudate in adult rats after intracerebral hemorrhage (ICH). Double immunofluorescence staining revealed that EHD2 was colocalized with neurons and activated microglias after ICH. Besides, we detected that neuronal apoptosis markers (TUNEL and caspase-3), and microglial activation marker (CD68), also known as a marker of macrophage, were colocated with EHD2. The vitro study also indicated that EHD2 was linked with neuronal apoptosis and microglial phagocytosis. All our findings suggested that EHD2 might be involved in the pathophysiology of ICH.
EHD2是Eps15同源结构域（EH结构域）家族的成员之一，在囊泡运输过程中的蛋白质相互作用中起重要作用。先前的研究已经证明，EHD2在胞吞作用过程中可调节从质膜的运输。然而，其在中枢神经系统疾病中的功能仍了解有限。在此背景下，我们发现脑出血（ICH）后成年大鼠血肿周围尾状核中EHD2表达上调。双重免疫荧光染色显示，ICH后EHD2与神经元和活化的小胶质细胞共定位。此外，我们检测到神经元凋亡标志物（TUNEL和caspase-3）以及小胶质细胞活化标志物（CD68，也称为巨噬细胞标志物）与EHD2共定位。体外研究还表明，EHD2与神经元凋亡和小胶质细胞吞噬作用有关。我们所有的研究结果表明，EHD2可能参与ICH的病理生理过程。
