TJP1 suppresses trophoblast cell invasion by expressing E2F8 in the human placenta

IF 3.8 3区 医学 Q2 CELL BIOLOGY Molecular and Cellular Endocrinology Pub Date : 2024-05-23 DOI:10.1016/j.mce.2024.112277
Rika Miki , Seiko Matsuo , Takafumi Ushida , Sho Tano , Kenji Imai , Akihiro Nawa , Hiroaki Kajiyama , Tomomi Kotani
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Abstract

Adequate extravillous trophoblast (EVT) invasion into the maternal decidua is important for human placental development. We identified that E2F transcription factor 8 (E2F8) suppresses EVT invasion, and that tight junction protein-1 (TJP1) is a potential downstream target gene of E2F8. We investigated the role of TJP1 in the human placenta and regulation of TJP1 expression by E2F8. TJP1 expression decreased in E2F8 knockdown HTR-8/SVneo cells. TJP1 and E2F8 were co-expressed in villi in the first-trimester placenta and in EVTs and villi in the third-trimester placenta. TJP1 was significantly increased in the pre-eclamptic compared with control placenta. TJP1 knockdown increased the invasion of HTR-8/SVneo cells, while TJP1 overexpression inhibited cell invasion. Halo-E2F8 overexpression significantly increased TJP1 expression and TJP1 transcription compared with control placenta. Our findings suggest that E2F8 promotes TJP1 transcription, and that TJP1 expression by E2F8 inhibits EVT invasion. TJP1 and E2F8 may be related to pre-eclampsia pathogenesis.

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TJP1 通过在人类胎盘中表达 E2F8 抑制滋养层细胞入侵
绒毛外滋养层细胞(EVT)充分侵入母体蜕膜对人类胎盘的发育非常重要。我们发现E2F转录因子8(E2F8)抑制EVT的侵入,而紧密连接蛋白-1(TJP1)是E2F8的潜在下游靶基因。我们研究了 TJP1 在人类胎盘中的作用以及 E2F8 对 TJP1 表达的调控。在 E2F8 敲除的 HTR-8/SVneo 细胞中,TJP1 的表达量减少。TJP1和E2F8在第一妊娠期胎盘的绒毛和第三妊娠期胎盘的EVT和绒毛中共同表达。与对照胎盘相比,子痫前期胎盘中的 TJP1 明显增加。敲除 TJP1 会增加 HTR-8/SVneo 细胞的侵袭,而过表达 TJP1 则会抑制细胞的侵袭。与对照胎盘相比,Halo-E2F8 过表达可显著增加 TJP1 的表达和 TJP1 的转录。我们的研究结果表明,E2F8能促进TJP1的转录,E2F8表达的TJP1能抑制EVT的侵袭。TJP1和E2F8可能与先兆子痫的发病机制有关。
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来源期刊
Molecular and Cellular Endocrinology
Molecular and Cellular Endocrinology 医学-内分泌学与代谢
CiteScore
9.00
自引率
2.40%
发文量
174
审稿时长
42 days
期刊介绍: Molecular and Cellular Endocrinology was established in 1974 to meet the demand for integrated publication on all aspects related to the genetic and biochemical effects, synthesis and secretions of extracellular signals (hormones, neurotransmitters, etc.) and to the understanding of cellular regulatory mechanisms involved in hormonal control.
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