Ren Jinlian, Cai Jing
Department of Obstetrics, Zhuji Affiliated Hospital of Wenzhou Medical University, Shaoxing, Zhejiang, China.
Department of Pathology, Shanghai Jiading District Anting Hospital, No. 1060 Hejing Road, Anting Town, Jiading District, Shanghai, China.
Open Med (Wars). 2023 Mar 1;18(1):20230645. doi: 10.1515/med-2023-0645. eCollection 2023.
Previous studies have indicated that the development of preeclampsia (PE) involves the regulation of circular RNA (circRNA). However, the role of hsa_circ_0014736 (circ_0014736) in PE remains unknown. Thus, the study proposes to reveal the function of circ_0014736 in the pathogenesis of PE and the underlying mechanism. The results showed that circ_0014736 and GPR4 expression were significantly upregulated, while miR-942-5p expression was downregulated in PE placenta tissues when compared with normal placenta tissues. circ_0014736 knockdown promoted the proliferation, migration, and invasion of placenta trophoblast cells (HTR-8/SVneo) and inhibited apoptosis; however, circ_0014736 overexpression had the opposite effects. circ_0014736 functioned as a sponge for miR-942-5p and regulated HTR-8/SVneo cell processes by interacting with miR-942-5p. Additionally, GPR4, a target gene of miR-942-5p, was involved in miR-942-5p-mediated actions in HTR-8/SVneo cells. Moreover, circ_0014736 stimulated GPR4 production through miR-942-5p. Collectively, circ_0014736 inhibited HTR-8/SVneo cell proliferation, migration, and invasion and induced cell apoptosis through the miR-942-5p/GPR4 axis, providing a possible target for the treatment of PE.
先前的研究表明,子痫前期(PE)的发展涉及环状RNA(circRNA)的调控。然而,hsa_circ_0014736(circ_0014736)在PE中的作用仍不清楚。因此,本研究旨在揭示circ_0014736在PE发病机制中的功能及潜在机制。结果显示,与正常胎盘组织相比,circ_0014736和GPR4在PE胎盘组织中的表达显著上调,而miR-942-5p的表达下调。敲低circ_0014736可促进胎盘滋养层细胞(HTR-8/SVneo)的增殖、迁移和侵袭,并抑制细胞凋亡;然而,circ_0014736过表达则产生相反的效果。circ_0014736作为miR-942-5p的海绵,通过与miR-942-5p相互作用来调节HTR-8/SVneo细胞的进程。此外,miR-942-5p的靶基因GPR4参与了miR-942-5p介导的HTR-8/SVneo细胞作用。而且,circ_0014736通过miR-942-5p刺激GPR4的产生。总的来说,circ_0014736通过miR-942-5p/GPR4轴抑制HTR-8/SVneo细胞的增殖、迁移和侵袭,并诱导细胞凋亡,为PE的治疗提供了一个可能的靶点。