Department of Obstetrics, Longhua District Maternity and Child Health Hospital, Shenzhen, Guangdong, China.
Department of Anesthesiology, Longhua District People's Hospital, Shenzhen, Guangdong, China.
Bioengineered. 2022 May;13(5):11456-11470. doi: 10.1080/21655979.2022.2066753.
Pre-eclampsia (PE) is a prevalent pregnancy disease characterized by insufficient trophoblast cell migration (HTR8/SVneo). Consequently, accelerating trophoblast cell proliferation might ameliorate PE. This study assessed the effects and molecular mechanisms of Sufentanil (SUF) on HTR8/SVneo cells proliferation. HTR8/SVneo cells and PE clinical samples were used. Peripheral blood was collected from PE patients' samples, and microRNA (miR)-24-3p and 11β-hydroxysteroid dehydrogenase type 2 (HSD11B2) was analyzed in the blood and cells. HTR8/SVneo cells were treated with varying SUF concentrations or transfected with miR-24-3p mimics/inhibitors, or HSD11B2 elevation vector. CCK-8, colony formation, transwell, and flow cytometry assays were then carried out. Association of miR-24 - 3p with HSD11B2 was investigated. PE animal model was constructed using Wistar rats to verify SUF's role on PE . According to the results, SUF boosted HTR8/SVneo cell proliferation, and inhibited miR-24-3p to accelerate HSD11B2. MiR-24-3p was increased in PE, while HSD11B2 was inhibited, and miR-24-3p targeted HSD11B2. HSD11B2 reversed miR-24-3p's repression on HTR/SVneo cell advancement. SUF restrained PE's progression in and in via mediating the miR-24-3p/HSD11B2 axis. In conclusion, SUF enhances HSD11B2 via repressing miR-24-3p, thereby suppressing PE's progression. The study provides an insight into the possibility of using SUF as a novel therapeutic target for PE, which acts via combining with miR-24-3p.
子痫前期 (PE) 是一种常见的妊娠疾病，其特征是滋养细胞迁移不足 (HTR8/SVneo)。因此，加速滋养细胞增殖可能改善 PE。本研究评估了舒芬太尼 (SUF) 对 HTR8/SVneo 细胞增殖的影响及其分子机制。使用 HTR8/SVneo 细胞和 PE 临床样本。从 PE 患者样本中采集外周血，并分析血液和细胞中的微小 RNA (miR)-24-3p 和 11β-羟类固醇脱氢酶 2 (HSD11B2)。用不同浓度的 SUF 处理 HTR8/SVneo 细胞，或用 miR-24-3p 模拟物/抑制剂或 HSD11B2 升高载体转染。然后进行 CCK-8、集落形成、transwell 和流式细胞术检测。研究了 miR-24-3p 与 HSD11B2 的相关性。使用 Wistar 大鼠构建 PE 动物模型，以验证 SUF 在 PE 中的作用。结果表明，SUF 促进 HTR8/SVneo 细胞增殖，并抑制 miR-24-3p 以加速 HSD11B2。PE 中 miR-24-3p 增加，而 HSD11B2 受到抑制，miR-24-3p 靶向 HSD11B2。HSD11B2 逆转了 miR-24-3p 对 HTR/SVneo 细胞进展的抑制作用。SUF 通过调节 miR-24-3p/HSD11B2 轴抑制 PE 在体内和体内的进展。总之，SUF 通过抑制 miR-24-3p 增强 HSD11B2，从而抑制 PE 的进展。该研究为使用 SUF 作为一种新的治疗 PE 的靶点提供了新的思路，其作用机制可能是与 miR-24-3p 结合。
