Apgujung St. Mary's Eye Center, Seoul, Republic of Korea.
Department of Ophthalmology, Hallym University Sacred Heart Hospital, Anyang, Republic of Korea.
PLoS One. 2022 Aug 31;17(8):e0273674. doi: 10.1371/journal.pone.0273674. eCollection 2022.
The abnormal posterior vitreous detachment (PVD) is speculated as an important mechanism of the development of the epiretinal membrane (ERM). However, there is only limited information about the molecular mechanism. Sphingosine-1-phosphate (S1P) is a mediator of the mechanosensitive response in several cell types that may have a role in the pathogenesis of ERM during abnormal PVD. Therefore, we evaluated the expression of S1P in the human ERM and the role of S1P in cultured human Muller glial cells. Among 24 ERM specimens, seven specimens (29.2%) exhibited S1P expression. Patients with secondary ERM or ellipsoid zone defects, which suggest abnormal PVD presented a significantly higher S1P+ cell density (secondary ERM: 128.20 ± 135.61 and 9.68 ± 36.01 cells, p = 0.002; EZ defects: 87.56 ± 117.79 vs 2.80 ± 8.85, p = 0.036). The addition of S1P increased the migrative ability and expression of N-cadherin and α-SMA in human Muller glial cells, suggesting S1P is a potential causative molecule for the development of ERM during abnormal PVD.
异常的玻璃体后脱离 (PVD) 被推测是发生视网膜内表面膜 (ERM) 的重要机制。然而，关于其分子机制的信息有限。鞘氨醇-1-磷酸 (S1P) 是几种细胞类型中机械敏感性反应的介质，在异常 PVD 期间 ERM 的发病机制中可能具有作用。因此，我们评估了 S1P 在人 ERM 中的表达及其在培养的人 Muller 胶质细胞中的作用。在 24 个 ERM 标本中，有 7 个标本（29.2%）表现出 S1P 表达。提示异常 PVD 的继发性 ERM 或椭圆体带缺陷患者的 S1P+细胞密度显著更高（继发性 ERM：128.20 ± 135.61 和 9.68 ± 36.01 个细胞，p = 0.002；EZ 缺陷：87.56 ± 117.79 与 2.80 ± 8.85，p = 0.036）。S1P 的加入增加了人 Muller 胶质细胞的迁移能力和 N-钙粘蛋白和 α-SMA 的表达，表明 S1P 是异常 PVD 期间 ERM 发展的潜在致病分子。
