Suppr超能文献

转录组分析揭示了马胎盘炎期间子宫肌激活的关键调节因子和分子机制。

Transcriptomic analysis reveals the key regulators and molecular mechanisms underlying myometrial activation during equine placentitis†.

机构信息

Maxwell H. Gluck Equine Research Center, Department of Veterinary Science, University of Kentucky, Lexington, Kentucky, USA.

Theriogenology Department, Faculty of Veterinary Medicine, University of Mansoura, Dakahlia, Mansoura, Egypt.

出版信息

Biol Reprod. 2020 May 26;102(6):1306-1325. doi: 10.1093/biolre/ioaa020.

Abstract

The key event in placentitis-induced preterm labor is myometrial activation with the subsequent initiation of labor. However, the molecular mechanisms underlying myometrial activation are not fully understood in the mares. Therefore, the equine myometrial transcriptome was characterized during placentitis (290.0 ± 1.52 days of GA, n = 5) and the prepartum period (330 days of GA, n = 3) in comparison to normal pregnant mares (289.8 ± 2.18 days of GA, n = 4). Transcriptome analysis identified 596 and 290 DEGs in the myometrium during placentitis and the prepartum period, respectively, with 138 DEGs in common. The placentitis DEGs included eight genes (MMP1, MMP8, S100A9, S100A8, PI3, APOBEC3Z1B, RETN, and CXCL2) that are exclusively expressed in the inflamed myometrium. Pathway analysis elucidated that inflammatory signaling, Toll-like receptor signaling, and apoptosis pathways dominate myometrial activation during placentitis. The prepartum myometrium was associated with overexpression of inflammatory signaling, oxidative stress, and 5-hydroxytryptamine degradation. Gene ontology enrichment analysis identified several chemoattractant factors in the myometrium during placentitis and prepartum period, including CCL2, CXCL1, CXCL3, and CXCL6 in common. Upstream regulator analysis revealed 19 potential upstream regulators in placentitis dataset including transcription regulators (E2F1, FOXM1, HIF1A, JUNB, NFKB1A, and STAT1), transmembrane receptors (FAS, ICAM1, SELP, TLR2, and TYROBP), growth factors (HGF and TGFB3), enzymes (PTGS2 and PRKCP), and others (S100A8, S100A9, CD44, and C5AR1). Additionally, three upstream regulators (STAT3, EGR1, and F2R) were identified in the prepartum dataset. These findings revealed the key regulators and pathways underlying myometrial activation during placentitis, which aid in understanding the disease and facilitate the development of efficacious therapies.

摘要

胎盘炎诱导早产的关键事件是子宫肌层激活,随后引发分娩。然而,在马中,子宫肌层激活的分子机制尚不完全清楚。因此,在胎盘炎(GA 290.0±1.52 天,n=5)和产前阶段(GA 330 天,n=3)中,对马的子宫肌层转录组进行了描述,并与正常妊娠马(GA 289.8±2.18 天,n=4)进行了比较。转录组分析分别在胎盘炎和产前阶段发现了 596 个和 290 个差异表达基因,其中有 138 个差异表达基因是共同的。胎盘炎的差异表达基因包括 8 个基因(MMP1、MMP8、S100A9、S100A8、PI3、APOBEC3Z1B、RETN 和 CXCL2),它们仅在发炎的子宫肌层中表达。通路分析表明,炎症信号、Toll 样受体信号和细胞凋亡通路在胎盘炎时主导子宫肌层激活。产前的子宫肌层与炎症信号、氧化应激和 5-羟色胺降解过度表达有关。基因本体富集分析在胎盘炎和产前期间的子宫肌层中鉴定了几种趋化因子,包括 CCL2、CXCL1、CXCL3 和 CXCL6。上游调控因子分析显示,胎盘炎数据集中有 19 个潜在的上游调控因子,包括转录调控因子(E2F1、FOXM1、HIF1A、JUNB、NFKB1A 和 STAT1)、跨膜受体(FAS、ICAM1、SELP、TLR2 和 TYROBP)、生长因子(HGF 和 TGFB3)、酶(PTGS2 和 PRKCP)和其他(S100A8、S100A9、CD44 和 C5AR1)。此外,在产前数据集还鉴定了三个上游调控因子(STAT3、EGR1 和 F2R)。这些发现揭示了胎盘炎时子宫肌层激活的关键调控因子和通路,有助于理解该疾病并促进有效治疗方法的开发。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验