Langert Kelly A, Pervan Cynthia L, Stubbs Evan B
Research Service; Department of Veterans Affairs; Edward Hines Jr. VA Hospital; Hines, IL USA; Neuroscience Institute; Stritch School of Medicine; Loyola University Chicago; Maywood, IL USA; Department of Ophthalmology; Stritch School of Medicine; Loyola University Chicago; Maywood, IL USA.
Small GTPases. 2014;5. doi: 10.4161/sgtp.29260. Epub 2014 Jun 9.
Transendothelial migration of autoreactive leukocytes into peripheral nerves is an early pathological hallmark of acute inflammatory demyelinating polyneuropathy (AIDP), a North American and European variant of Guillain-Barré Syndrome. Whereas the clinical management of AIDP is currently limited to non-selective immune modulating therapies, recent experimental studies support selective targeting of leukocyte trafficking as a promising alternative therapeutic strategy. Here, using a combination of targeted siRNA knockdown and pharmacological inhibitors, we report a novel role of both Cdc42 and RalA GTPases in facilitating TNF-α mediated CCL2 trafficking and release from immortalized rat peripheral nerve microvascular endoneurial endothelial cells. These findings raise interest in Cdc42 and RalA GTPases as potential therapeutic targets for the management of autoimmune inflammatory peripheral nerve disease.
自身反应性白细胞经内皮迁移至周围神经是急性炎症性脱髓鞘性多发性神经病(AIDP)的早期病理特征,AIDP是格林-巴利综合征在北美和欧洲的变体。虽然目前AIDP的临床治疗仅限于非选择性免疫调节疗法,但最近的实验研究支持将白细胞迁移作为一种有前景的替代治疗策略进行选择性靶向治疗。在此,我们使用靶向小干扰RNA敲低和药理学抑制剂相结合的方法,报告了Cdc42和RalA GTP酶在促进肿瘤坏死因子-α介导的CCL2从永生化大鼠周围神经微血管内膜内皮细胞转运和释放中的新作用。这些发现引发了人们对Cdc42和RalA GTP酶作为自身免疫性炎性周围神经病治疗潜在靶点的兴趣。