Laboratory of Molecular and Cellular Pharmacology of Purinergic Transmission, Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Via Balzaretti 9, 20133, Milan, Italy.
Adv Exp Med Biol. 2017;1051:169-192. doi: 10.1007/5584_2017_92.
In 2006, cells heterologously expressing the "orphan" receptor GPR17 were shown to acquire responses to both uracil nucleotides and cysteinyl-leukotrienes, two families of signaling molecules accumulating in brain or heart as a result of hypoxic/traumatic injuries. In subsequent years, evidence of GPR17 key role in oligodendrogenesis and myelination has highlighted it as a "model receptor" for new therapies in demyelinating and neurodegenerative diseases. The apparently contrasting evidence in the literature about the role of GPR17 in promoting or inhibiting myelination can be due to its transient expression in the intermediate stages of differentiation, exerting a pro-differentiating function in early oligodendrocyte precursor cells (OPCs), and an inhibitory role in late stage maturing cells. Meanwhile, several papers extended the initial data on GPR17 pharmacology, highlighting a "promiscuous" behavior of this receptor; indeed, GPR17 is able to respond to other emergency signals like oxysterols or the pro-inflammatory cytokine SDF-1, underlying GPR17 ability to adapt its responses to changes of the surrounding extracellular milieu, including damage conditions. Here, we analyze the available literature on GPR17, in an attempt to summarize its emerging biological roles and pharmacological properties.
2006 年,研究表明,异源表达“孤儿”受体 GPR17 的细胞能够对尿嘧啶核苷酸和半胱氨酰白三烯两种信号分子家族产生反应,这两种信号分子家族在缺氧/创伤性损伤后会在大脑或心脏中积累。在随后的几年中,GPR17 在少突胶质细胞发生和髓鞘形成中的关键作用的证据突出了它作为脱髓鞘和神经退行性疾病新疗法的“模型受体”。文献中关于 GPR17 在促进或抑制髓鞘形成中的作用的明显矛盾的证据可能是由于其在分化的中间阶段短暂表达,在早期少突胶质前体细胞 (OPC) 中发挥促分化功能,在晚期成熟细胞中发挥抑制作用。同时,有几篇论文扩展了 GPR17 药理学的初始数据,突出了该受体的“混杂”行为;事实上,GPR17 能够对其他紧急信号(如氧化固醇或促炎细胞因子 SDF-1)产生反应,这表明 GPR17 能够根据周围细胞外环境(包括损伤条件)的变化来调整其反应。在这里,我们分析了 GPR17 的现有文献,试图总结其新兴的生物学作用和药理学特性。