State Key Laboratory of Drug Research, National Center for Drug Screening, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
School of Pharmacy, University of Chinese Academy of Sciences, Beijing, 100049, China.
Acta Pharmacol Sin. 2024 Mar;45(3):490-501. doi: 10.1038/s41401-023-01183-7. Epub 2023 Nov 7.
Oligodendrocytes (OLs) are glial cells that ensheath neuronal axons and form myelin in the central nervous system (CNS). OLs are differentiated from oligodendrocyte precursor cells (OPCs) during development and myelin repair, which is often insufficient in the latter case in demyelinating diseases such as multiple sclerosis (MS). Many factors have been reported to regulate OPC-to-OL differentiation, including a number of G protein-coupled receptors (GPCRs). In an effort to search pathways downstream of GPCRs that might be involved in OPC differentiation, we discover that U73122, a phosphoinositide specific phospholipase C (PI-PLC) inhibitor, dramatically promotes OPC-to-OL differentiation and myelin regeneration in experimental autoimmune encephalomyelitis model. Unexpectedly, U73343, a close analog of U73122 which lacks PI-PLC inhibitory activity also promotes OL differentiation, while another reported PI-PLC inhibitor edelfosine does not have such effect, suggesting that U73122 and U73343 enhance OPC differentiation independent of PLC. Although the structures of U73122 and U73343 closely resemble 17β-estradiol, and both compounds do activate estrogen receptors Erα and Erβ with low efficacy and potency, further study indicates that these compounds do not act through Erα and/or Erβ to promote OPC differentiation. RNA-Seq and bioinformatic analysis indicate that U73122 and U73343 may regulate cholesterol biosynthesis. Further study shows both compounds increase 14-dehydrozymostenol, a steroid reported to promote OPC differentiation, in OPC culture. In conclusion, the aminosteroids U73122 and U73343 promote OPC-to-OL generation and myelin formation by regulating cholesterol biosynthesis pathway.
少突胶质细胞(OLs)是包裹神经元轴突并在中枢神经系统(CNS)中形成髓鞘的神经胶质细胞。OLs 在发育和髓鞘修复过程中从少突胶质前体细胞(OPCs)分化而来,在后一种情况下,髓鞘脱失性疾病(如多发性硬化症(MS))往往不足。已经报道了许多因素来调节 OPC 向 OL 的分化,包括许多 G 蛋白偶联受体(GPCRs)。为了寻找可能参与 OPC 分化的 GPCR 下游途径,我们发现 U73122,一种磷脂酰肌醇特异性磷脂酶 C(PI-PLC)抑制剂,在实验性自身免疫性脑脊髓炎模型中显著促进 OPC 向 OL 的分化和髓鞘再生。出乎意料的是,U73343,一种缺乏 PI-PLC 抑制活性的 U73122 的紧密类似物,也促进 OL 分化,而另一种报道的 PI-PLC 抑制剂埃达福司汀则没有这种作用,这表明 U73122 和 U73343 增强 OPC 分化独立于 PLC。尽管 U73122 和 U73343 的结构与 17β-雌二醇非常相似,并且这两种化合物都以低效力和效力激活雌激素受体 Erα 和 Erβ,但进一步的研究表明,这些化合物不是通过 Erα 和/或 Erβ 起作用来促进 OPC 分化。RNA-Seq 和生物信息学分析表明,U73122 和 U73343 可能调节胆固醇生物合成。进一步的研究表明,这两种化合物在 OPC 培养物中增加了 14-脱氢胆固醇,一种报道能促进 OPC 分化的甾体。总之,氨基甾体 U73122 和 U73343 通过调节胆固醇生物合成途径促进 OPC 向 OL 的产生和髓鞘形成。