Perinatology Research Branch, Division of Obstetrics and Maternal-Fetal Medicine, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Department of Health and Human Services (NICHD/NIH/DHHS), Detroit, MI 48201, USA; Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI 48201, USA.
Perinatology Research Branch, Division of Obstetrics and Maternal-Fetal Medicine, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Department of Health and Human Services (NICHD/NIH/DHHS), Detroit, MI 48201, USA; Department of Obstetrics and Gynecology, University of Michigan, Ann Arbor, MI 48109, USA; Department of Epidemiology and Biostatistics, Michigan State University, East Lansing, MI 48824, USA; Center for Molecular Medicine and Genetics, Wayne State University, Detroit, MI 48201, USA; Detroit Medical Center, Detroit, MI 48201, USA.
Cell Rep. 2023 Jan 31;42(1):111846. doi: 10.1016/j.celrep.2022.111846. Epub 2023 Jan 3.
Preterm birth, the leading cause of perinatal morbidity and mortality worldwide, frequently results from the syndrome of preterm labor. The best-established causal link to preterm labor is intra-amniotic infection, which involves premature activation of the parturition cascade in the reproductive tissues. Herein, we utilize single-cell RNA sequencing (scRNA-seq) to generate a single-cell atlas of the murine uterus, decidua, and cervix in a model of infection-induced preterm labor. We show that preterm labor affects the transcriptomic profiles of specific immune and non-immune cell subsets. Shared and tissue-specific gene expression signatures are identified among affected cells. Determination of intercellular communications implicates specific cell types in preterm labor-associated signaling pathways across tissues. In silico comparison of murine and human uterine cell-cell interactions reveals conserved signaling pathways implicated in labor. Thus, our scRNA-seq data provide insights into the preterm labor-driven cellular landscape and communications in reproductive tissues.
早产是全球围产期发病率和死亡率的主要原因，通常由早产劳动综合征引起。与早产劳动最密切相关的因果关系是羊膜内感染，它涉及生殖组织中分娩级联的过早激活。在这里，我们利用单细胞 RNA 测序（scRNA-seq）在感染诱导的早产劳动模型中生成小鼠子宫、蜕膜和宫颈的单细胞图谱。我们表明，早产劳动会影响特定免疫和非免疫细胞亚群的转录组谱。受影响细胞之间存在共享和组织特异性基因表达特征。细胞间通讯的确定表明，特定细胞类型参与了跨组织的与早产劳动相关的信号通路。对鼠类和人类子宫细胞-细胞相互作用的计算机模拟比较揭示了与劳动相关的保守信号通路。因此，我们的 scRNA-seq 数据为生殖组织中早产劳动驱动的细胞景观和通讯提供了深入了解。
