Placenta · 2026
Mechanistic study of miR-486-5p targeting Claudin-10 in placenta accreta spectrum pathogenesis and its impact on trophoblast behavior.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Dong Tian, Jiang Ying, Ye Fenglei, Zhao Baihui, Xi Fangfang, Lv Min, Yang Mengmeng, Pu Yuqun, Jiang Peiyue, Luo Qiong
Аннотация
INTRODUCTION: Placenta accreta spectrum (PAS) is a severe pregnancy complication characterized by abnormal invasion of trophoblasts into the myometrium. Despite improved diagnosis, its molecular mechanisms remain unclear. Emerging evidence highlights microRNAs in regulating epithelial-mesenchymal transition (EMT). Here, we focus on miR-486-5p and its target Claudin-10 to explore their roles in PAS pathogenesis.
METHODS: Placental tissues from 40 PAS patients and 40 controls were collected. RNA-seq was performed in an exploratory subset of five paired implanted and adjacent non-implanted tissues from PAS cases, and key candidates were validated in the full cohort by qRT-PCR, IHC, and Western blot. A ceRNA network was constructed to identify key regulators. Functional assays, including luciferase reporter, transwell migration/invasion, and wound healing, were performed in HTR-8/SVneo cells.
RESULTS: Transcriptomic profiling revealed miR-486-5p as a central regulator, significantly upregulated in PAS tissues, with expression correlating with disease severity. Claudin-10 was downregulated and inversely correlated with miR-486-5p levels. Functional assays demonstrated that miR-486-5p promoted trophoblast migration and invasion by directly targeting Claudin-10, thereby inducing EMT. Rescue experiments confirmed Claudin-10 as the critical downstream effector of miR-486-5p.
DISCUSSION: Our findings identify the miR-486-5p/Claudin-10 axis as a novel regulator of trophoblast invasiveness in PAS through EMT modulation. This pathway provides new insights into PAS pathogenesis and may serve as a potential biomarker and therapeutic target.
METHODS: Placental tissues from 40 PAS patients and 40 controls were collected. RNA-seq was performed in an exploratory subset of five paired implanted and adjacent non-implanted tissues from PAS cases, and key candidates were validated in the full cohort by qRT-PCR, IHC, and Western blot. A ceRNA network was constructed to identify key regulators. Functional assays, including luciferase reporter, transwell migration/invasion, and wound healing, were performed in HTR-8/SVneo cells.
RESULTS: Transcriptomic profiling revealed miR-486-5p as a central regulator, significantly upregulated in PAS tissues, with expression correlating with disease severity. Claudin-10 was downregulated and inversely correlated with miR-486-5p levels. Functional assays demonstrated that miR-486-5p promoted trophoblast migration and invasion by directly targeting Claudin-10, thereby inducing EMT. Rescue experiments confirmed Claudin-10 as the critical downstream effector of miR-486-5p.
DISCUSSION: Our findings identify the miR-486-5p/Claudin-10 axis as a novel regulator of trophoblast invasiveness in PAS through EMT modulation. This pathway provides new insights into PAS pathogenesis and may serve as a potential biomarker and therapeutic target.