Department of Obstetrics and Gynecology, Maternity Hospital Affiliated to Nanjing Medical University, Nanjing, Jiangsu 210004, P.R. China.
Obstetric Ward II, The Affiliated Northwest Women's and Children's Hospital of Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi 710061, P.R. China.
Mol Med Rep. 2022 Apr;25(4). doi: 10.3892/mmr.2022.12631. Epub 2022 Feb 9.
Pentraxin 3 (PTX3), a member of the c‑reactive protein family, is a long pentraxin protein and a pro‑inflammatory marker. However, the role of PTX3 in preeclampsia (PE) remains to be elucidated. Thus, the present study aimed to investigate the biological role and mechanisms underlying PTX3 in PE. In the present study, PTX3 was overexpressed in trophoblasts and the subsequent changes in cell proliferation, cycle distribution and invasion were observed using Cell Counting Kit‑8, flow cytometry and Transwell assays, respectively. Moreover, the expression levels of MMP2 and MMP9, proteins associated with the development of PE, were detected using reverse transcription‑quantitative PCR and western blot analysis. Following treatment with interleukin (IL)‑1β, the expression levels of PTX3 were measured. Furthermore, subsequent changes in cell proliferation, cycle distribution and invasion were investigated following overexpression of PTX3 and treatment with IL‑1 receptor antagonist (IL‑1Ra). Overexpression of PTX3 inhibited the proliferation, cycle and invasion of HTR‑8/SV neo and JEG3 cells. Moreover, treatment with IL‑1β increased the expression of PTX3 in HTR‑8/SV neo and JEG3 cells, which was suppressed following treatment with the IL‑1β antagonist. Following PTX3 overexpression and treatment with IL‑1Ra, the inhibitory effects of PTX3 overexpression alone on the invasion of HTR‑8/SV neo and JEG3 cells were attenuated. In conclusion, these results indicated that IL‑1β could induce PTX3 upregulation, which led to the inhibition of the proliferation, invasion and cell cycle of trophoblasts, thereby promoting the progression of PE.
五聚素 3(PTX3)是 C 反应蛋白家族的一员,是一种长五聚素蛋白和促炎标志物。然而,PTX3 在子痫前期(PE)中的作用仍有待阐明。因此,本研究旨在探讨 PTX3 在 PE 中的生物学作用和机制。在本研究中,通过细胞计数试剂盒-8 检测、流式细胞术和 Transwell 分析分别观察到在滋养细胞中过表达 PTX3 后细胞增殖、细胞周期分布和侵袭的变化。此外,使用逆转录-定量 PCR 和蛋白质印迹分析检测与 PE 发展相关的 MMP2 和 MMP9 蛋白的表达水平。用白细胞介素(IL)-1β处理后,检测 PTX3 的表达水平。此外,过表达 PTX3 并给予 IL-1 受体拮抗剂(IL-1Ra)处理后,观察细胞增殖、细胞周期分布和侵袭的变化。PTX3 的过表达抑制了 HTR-8/SV neo 和 JEG3 细胞的增殖、周期和侵袭。此外,IL-1β 处理增加了 HTR-8/SV neo 和 JEG3 细胞中 PTX3 的表达,而用 IL-1β 拮抗剂处理后则抑制了其表达。过表达 PTX3 并给予 IL-1Ra 处理后,PTX3 过表达单独对 HTR-8/SV neo 和 JEG3 细胞侵袭的抑制作用减弱。综上所述,这些结果表明,IL-1β 可诱导 PTX3 上调,从而抑制滋养细胞的增殖、侵袭和细胞周期,促进 PE 的进展。