Gofrit Shany G, Shavit-Stein Efrat
Department of Neurology and Joseph Sagol Neuroscience Center, Sheba Medical Center, Tel Hashomer, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Neural Regen Res. 2019 Dec;14(12):2043-2053. doi: 10.4103/1673-5374.262568.
The neuro-glial interface extends far beyond mechanical support alone and includes interactions throu-gh coagulation cascade proteins. Here, we systematically review the evidence indicating that synaptic and node of Ranvier glia cell components modulate synaptic transmission and axonal conduction by a coagulation cascade protein system, leading us to propose the concept of the neuro-glial coagulonome. In the peripheral nervous system, the main thrombin receptor protease activated receptor 1 (PAR1) is located on the Schwann microvilli at the node of Ranvier and at the neuromuscular junction. PAR1 activation effects can be both neuroprotective or harmful, depending on thrombin activity levels. Low physiological levels of thrombin induce neuroprotective effects in the Schwann cells which are mediated by the endothelial protein C receptor. High levels of thrombin induce conduction deficits, as found in experimental autoimmune neuritis, the animal model for Guillaine-Barre syndrome. In the central nervous system, PAR1 is located on the peri-synaptic astrocyte end-feet. Its activation by high thrombin levels is involved in the pathology of primary inflammatory brain diseases such as multiple sclerosis, as well as in other central nervous system insults, including trauma, neoplasms, epilepsy and vascular injury. Following activation of PAR1 by high thrombin levels the seizure threshold is lowered. On the other hand, PAR1 activation by lower levels of thrombin in the central nervous system protects against a future ischemic insult. This review presents the known structure and function of the neuro-glial coagulonome, focusing on coagulation, thrombin and PAR1 in a pathway which may be either physiological (neuroprotective) or detrimental in peripheral nervous system and central nervous system diseases. Understanding the neuro-glial coagulonome may open opportunities for novel pharmacological interventions in neurological diseases.
神经胶质界面的作用远不止于单纯的机械支持,还包括通过凝血级联蛋白的相互作用。在此,我们系统地回顾了证据,表明郎飞结处的突触和神经胶质细胞成分通过凝血级联蛋白系统调节突触传递和轴突传导,从而促使我们提出神经胶质凝血组的概念。在周围神经系统中,主要的凝血酶受体蛋白酶激活受体1(PAR1)位于郎飞结处的施万细胞微绒毛以及神经肌肉接头处。PAR1激活效应可能是神经保护性的,也可能是有害的,这取决于凝血酶的活性水平。低生理水平的凝血酶在施万细胞中诱导神经保护作用,这种作用由内皮蛋白C受体介导。高凝血酶水平会导致传导缺陷,如在实验性自身免疫性神经炎(格林-巴利综合征的动物模型)中所见。在中枢神经系统中,PAR1位于突触周围星形胶质细胞的终足上。高凝血酶水平对其激活参与了原发性炎症性脑疾病(如多发性硬化症)的病理过程,以及其他中枢神经系统损伤,包括创伤、肿瘤、癫痫和血管损伤。高凝血酶水平激活PAR1后会降低癫痫阈值。另一方面,中枢神经系统中较低水平的凝血酶激活PAR1可预防未来的缺血性损伤。本综述介绍了神经胶质凝血组的已知结构和功能,重点关注凝血、凝血酶和PAR1在一条可能在周围神经系统和中枢神经系统疾病中具有生理(神经保护)或有害作用的途径中的情况。了解神经胶质凝血组可能为神经疾病的新型药物干预开辟机会。