RNA 测序揭示了小鼠模型中子宫内膜异位症病变发展的新分子机制。

IF 4 3区 医学 Q2 CELL BIOLOGY
Disease Models & Mechanisms Pub Date : 2024-10-01 Epub Date: 2024-10-23 DOI:10.1242/dmm.050566
Kavita Panir, John E Schjenken, James Breen, Hon Yeung Chan, Erin Greaves, Sarah A Robertson, M Louise Hull
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引用次数: 0

摘要

对子宫内膜异位症病理生理学的分子机制以及病变形成的上游驱动因素的了解仍然有限。我们使用一种 C57Bl/6 小鼠模型,将蜕膜化的子宫内膜组织皮下注射到受体小鼠的腹部,在蜕膜化的子宫内膜组织(4 个)以及子宫内膜异位症样病变形成的第 7 天(4 个)和第 14 天(4 个),我们建立了一个全面的基因表达谱。通过高通量 mRNA 测序,我们确定了参与子宫内膜异位症样病变发生和发展的基因和通路。我们观察到了不同的基因表达模式,病变和蜕膜化子宫内膜之间存在很大差异,且在两个病变时间点上保持稳定,这与人类子宫内膜异位症病变形成过程中的转录变化相似。通路富集分析揭示了几条与免疫和炎症反应相关的典型通路、多个潜在的上游调控因子,以及包括 IRF2BP2 和 ZBTB10 在内的以前未涉及子宫内膜异位症发病机制的基因的参与,表明这些基因在疾病进展中扮演着新的角色。总之,所提供的数据将成为研究该小鼠模型中子宫内膜异位症样病变发生的分子机制的有用资源。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
RNA sequencing reveals molecular mechanisms of endometriosis lesion development in mice.

Understanding of molecular mechanisms contributing to the pathophysiology of endometriosis, and upstream drivers of lesion formation, remains limited. Using a C57Bl/6 mouse model in which decidualized endometrial tissue is injected subcutaneously in the abdomen of recipient mice, we generated a comprehensive profile of gene expression in decidualized endometrial tissue (n=4), and in endometriosis-like lesions at Day 7 (n=4) and Day 14 (n=4) of formation. High-throughput mRNA sequencing allowed identification of genes and pathways involved in the initiation and progression of endometriosis-like lesions. We observed distinct patterns of gene expression with substantial differences between the lesions and the decidualized endometrium that remained stable across the two lesion timepoints, and showed similarity to transcriptional changes implicated in human endometriosis lesion formation. Pathway enrichment analysis revealed several immune and inflammatory response-associated canonical pathways, multiple potential upstream regulators, and involvement of genes not previously implicated in endometriosis pathogenesis, including IRF2BP2 and ZBTB10, suggesting novel roles in disease progression. Collectively, the provided data will be a useful resource to inform research on the molecular mechanisms contributing to endometriosis-like lesion development in this mouse model.

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来源期刊
Disease Models & Mechanisms
Disease Models & Mechanisms 医学-病理学
CiteScore
6.60
自引率
7.00%
发文量
203
审稿时长
6-12 weeks
期刊介绍: Disease Models & Mechanisms (DMM) is an online Open Access journal focusing on the use of model systems to better understand, diagnose and treat human disease.
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