Department of Obstetrics, Maternal and Child Health Hospital of Hubei Province, Wuhan, Hubei, China.
Department of Gynaecology, Maternal and Child Health Hospital of Hubei Province, Wuhan, Hubei, China.
Clinics (Sao Paulo). 2022 Jun 6;77:100055. doi: 10.1016/j.clinsp.2022.100055. eCollection 2022.
Long non-coding RNAs (LncRNAs) act as an indispensable role in the Preeclampsia (PE)-related trophoblast function, while its relationship with Small Nucleolar RNA Host Gene 22 (SNHG22) remains unknown. Hence, this study aimed to investigate the roles of lncRNA SNHG22 in the Preeclampsia (PE)-related trophoblasts function and the underlying mechanism.
Normal placentas and placentas from PE patients were collected to detect the expression of lncRNA SNHG22. Then, trophoblasts HTR-8/Svneo and JEG-3 were purchased, cultured, and treated to investigate the roles of lncRNA SNHG22 on cell migration and invasion as well as its underlying regulatory mechanism.
The SNHG22 was downregulated in PE patients, and it was found that SNHG22 overexpression could drive migration and invasion of trophoblasts, while SNHG22 depletion exerted a suppressive effect. Mechanistically, SNHG22 was validated to regulate microRNA-128-3p (miR-128-3p), and Protocadherin 11 X-Linked (PCDH11X) was identified as the target gene of miR-128-3p. Furthermore, it was found that SNHG22 acted as a promoter in the migration and invasion of trophoblast cells in a miR-128-3p/PCDH11X dependent manner, and SNHG22 silencing weakened the activation of PCDH11X-mediated PI3K/Akt signaling pathways through inhibiting miR-128-3p, thereby preventing migration and invasion of trophoblasts.
SNHG22 acted as a driver in the migration and invasion of trophoblasts and may be considered a candidate for the amelioration of PE.
长链非编码 RNA（lncRNA）在子痫前期（PE）相关滋养细胞功能中发挥不可或缺的作用，但其与小核仁 RNA 宿主基因 22（SNHG22）的关系尚不清楚。因此，本研究旨在探讨 lncRNA SNHG22 在子痫前期（PE）相关滋养细胞功能中的作用及其潜在机制。
收集正常胎盘和 PE 患者胎盘，检测 lncRNA SNHG22 的表达。然后，购买、培养并处理滋养细胞 HTR-8/Svneo 和 JEG-3，以研究 lncRNA SNHG22 对细胞迁移和侵袭的作用及其潜在的调节机制。
PE 患者中 SNHG22 表达下调，发现 SNHG22 过表达可促进滋养细胞的迁移和侵袭，而 SNHG22 耗竭则发挥抑制作用。机制上，验证 SNHG22 可调节 microRNA-128-3p（miR-128-3p），并确定原钙黏蛋白 11X 连锁（PCDH11X）为 miR-128-3p 的靶基因。此外，发现 SNHG22 以 miR-128-3p/PCDH11X 依赖的方式在滋养细胞迁移和侵袭中起促进作用，SNHG22 沉默通过抑制 miR-128-3p 减弱 PCDH11X 介导的 PI3K/Akt 信号通路的激活，从而阻止滋养细胞的迁移和侵袭。
SNHG22 在滋养细胞的迁移和侵袭中起驱动作用，可作为改善 PE 的候选物。
