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ELF1/PRR11/ARP2/3 促进早孕滋养细胞的增殖和迁移。

ELF1/PRR11/ARP2/3 promoted trophoblast cells proliferation and motility in early pregnancy.

机构信息

Key Laboratory of Agricultural Animal Genetics, Breeding and Reproduction, Huazhong Agricultural University, Wuhan, Hubei, China.

Center for Reproductive Medicine, Children's Hospital of Shanxi and Women Health Center, Taiyuan, Shanxi, China.

出版信息

Am J Reprod Immunol. 2023 Sep;90(3):e13758. doi: 10.1111/aji.13758.

DOI:10.1111/aji.13758
PMID:37641376
Abstract

BACKGROUND/OBJECTIVE: Early pregnancy loss (EPL) is a common adverse pregnancy outcome with an incidence of approximately 10-30%. There are many factors that cause EPL, among which the lack of proliferation and invasive properties of trophoblast cells can lead to embryonic development. Therefore, in this study, the molecular biology of trophoblast cells was investigated.

METHODS

Placental villous tissues from EPL patients were collected to explore ELF1 and PRR11 gene expression. The proliferation and migration of trophoblast cells were assessed by MTT, crystalline violet staining, and traswell assays, respectively. Western blotting and RT-qPCR were performed to investigate the relationship between ELF1, PRR11, and ARP2/3. F-actin polymerization and FAK activation were evaluated by immunofluorescence and western blotting. Ultimately, ELF1/PRR11/ARP2/3 expression was verified in the EPL mice model RESULTS: ELF1 and PRR11 were lowly expressed in placental villous tissues from EPL. The overexpression of ELF1 and PRR11 promoted proliferation and migration of trophoblast cells. Moreover, while ELF1 bound to the PRR11 promoter and promoted transcriptional activation. Finally, ELF1/PRR11/ARP2/3 showed low expression in the placental tissue of EPL mice.

CONCLUSION

Our study suggested that PRR11 promoted the motility of trophoblast cells by binding to the ARP2/3 complex to promote F-actin polymerization and FAK activation. In addition, ELF1 bound to the initiation site of PRR11 to promote its transcription. ELF1/PRR11/ARP2/3 may play an important role in EPL.

摘要

背景/目的:早期妊娠丢失(EPL)是一种常见的不良妊娠结局,其发病率约为 10-30%。有许多因素可导致 EPL,其中滋养细胞的增殖和侵袭特性缺失可导致胚胎发育不良。因此,本研究探讨了滋养细胞的分子生物学。

方法

收集 EPL 患者的胎盘绒毛组织,探讨 ELF1 和 PRR11 基因的表达。通过 MTT、结晶紫染色和 Transwell 分析分别评估滋养细胞的增殖和迁移。通过 Western blot 和 RT-qPCR 研究 ELF1、PRR11 和 ARP2/3 之间的关系。通过免疫荧光和 Western blot 评估 F-肌动蛋白聚合和 FAK 激活。最终,在 EPL 小鼠模型中验证了 ELF1/PRR11/ARP2/3 的表达。

结果

ELF1 和 PRR11 在 EPL 胎盘绒毛组织中低表达。ELF1 和 PRR11 的过表达促进了滋养细胞的增殖和迁移。此外,ELF1 与 PRR11 启动子结合并促进转录激活。最后,ELF1/PRR11/ARP2/3 在 EPL 小鼠胎盘组织中低表达。

结论

本研究表明,PRR11 通过与 ARP2/3 复合物结合促进 F-肌动蛋白聚合和 FAK 激活,从而促进滋养细胞的迁移。此外,ELF1 结合到 PRR11 的起始位点以促进其转录。ELF1/PRR11/ARP2/3 可能在 EPL 中发挥重要作用。

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