Department of Obstetrics and Gynecology, The First People's Hospital of Wenling, Wenling, China.
Physiol Res. 2023 Nov 28;72(5):597-606. doi: 10.33549/physiolres.935131.
The development of preeclampsia (PE) is associated with the impaired trophoblast motility. MicroRNAs (miRs) contribute to the modulation of trophoblast invasion. In the current study, the role of miR-206/AGTR1 in the TNF-alpha-induced invasion defect of trophoblasts was explored. The levels of miR-206 and ATGR1 in clinical placenta tissues were investigated. Trophoblasts were treated with TNF-alpha, and the levels of miR-206 and ATGR1 were modulated. Changes in cell viability, invasion, and inflammation in trophoblasts were detected. The level of miR-206 was induced, while the level of AGTR1 was suppressed in placenta tissues. In in vitro assays, TNF-alpha suppressed viability, induced inflammatory response, inhibited invasion, upregulated miR-206, and down-regulated AGTR1. The inhibited expression of miR-206 or the overexpression of AGTR1 counteracted the effects of TNF-alpha, indicating the key role of the miR-206/AGTR1 in progression of PE. Collectively, miR-206 suppressed viability, induced inflammatory response, and decreased invasion of trophoblasts by inhibiting AGTR1.
子痫前期（PE）的发展与滋养细胞运动功能受损有关。微小 RNA（miRs）有助于调节滋养细胞的侵袭。在本研究中，探讨了 miR-206/AGTR1 在 TNF-α诱导的滋养细胞侵袭缺陷中的作用。研究了临床胎盘组织中 miR-206 和 ATGR1 的水平。用 TNF-α处理滋养细胞，并调节 miR-206 和 ATGR1 的水平。检测滋养细胞活力、侵袭和炎症的变化。miR-206 的水平升高，而胎盘组织中 AGTR1 的水平降低。在体外实验中，TNF-α抑制活力，诱导炎症反应，抑制侵袭，上调 miR-206，并下调 AGTR1。miR-206 表达抑制或 AGTR1 过表达可逆转 TNF-α的作用，表明 miR-206/AGTR1 在 PE 的进展中起关键作用。总之，miR-206 通过抑制 AGTR1 抑制滋养细胞活力、诱导炎症反应和减少侵袭。
