Abstract Preeclampsia (PE) is a specific disorder of pregnancy with significant morbidity and mortality to the mother and the fetus. It has been reported that abnormal regulation of trophoblast cells contributes to the development of PE. LIM and SH3 Protein 2 (LASP2) belongs to nebulin protein family of actin-binding protein that has broad biological functions. In this study, we evaluated the role of LASP2 in the regulation of trophoblast cells. Our results demonstrated that LASP2 was markedly up-regulated in the placentas of patients with PE. Overexpression of LASP2 significantly suppressed the cell proliferation, migration, and invasion of trophoblast cells. LASP2 overexpression reduced the expression levels of β-catenin, cyclin D1, and c-Myc in trophoblast cells. Furthermore, activation of Wnt/β-catenin pathway booked the effects of LASP2 on trophoblast cells. In conclusion, these findings indicated that LASP2 might contribute to the pathogenesis of PE via regulating cell proliferation, migration, and invasion of trophoblast cells. Thus, LASP2 might be a prospective therapeutic target for the prevention and treatment of PE.

中文翻译：

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LASP2通过Wnt/β-catenin信号通路的失活抑制子痫前期滋养层细胞的迁移和侵袭

摘要 先兆子痫（PE）是一种特殊的妊娠疾病，对母体和胎儿的发病率和死亡率都很高。据报道，滋养层细胞的异常调节有助于 PE 的发展。LIM 和 SH3 蛋白 2 (LASP2) 属于具有广泛生物学功能的肌动蛋白结合蛋白的 nebulin 蛋白家族。在这项研究中，我们评估了 LASP2 在滋养层细胞调节中的作用。我们的结果表明 LASP2 在 PE 患者的胎盘中显着上调。LASP2的过表达显着抑制滋养层细胞的增殖、迁移和侵袭。LASP2 过表达降低了滋养层细胞中 β-连环蛋白、细胞周期蛋白 D1 和 c-Myc 的表达水平。此外，Wnt/β-catenin 通路的激活预定了 LASP2 对滋养层细胞的影响。总之，这些发现表明 LASP2 可能通过调节滋养层细胞的细胞增殖、迁移和侵袭来促进 PE 的发病机制。因此，LASP2 可能是预防和治疗 PE 的前瞻性治疗靶点。