Center of Translational Medicine for Maternal and Children's Health, Lianyungang Maternal and Children's Hospital, Lianyungang, Jiangsu, China.
PLoS One. 2013 Nov 27;8(11):e79897. doi: 10.1371/journal.pone.0079897. eCollection 2013.
Preterm birth (PTB) is a live birth delivered before 37 weeks of gestation (GW). About one-third of PTBs result from the preterm premature rupture of membranes (PPROM). Up to the present, the pathogenic mechanisms underlying PPROM are not clearly understood. Here, we investigated the differential expression of long chain non-coding RNAs (lncRNAs) in placentas of PTBs with PPROM, and their possible involvement in the pathogenic pathways leading to PPROM. A total number of 1954, 776, and 1050 lncRNAs were identified with a microarray from placentas of PPROM (group A), which were compared to full-term birth (FTB) (group B), PTB (group C), and premature rupture of membrane (PROM) (group D) at full-term, respectively. Instead of investigating the individual pathogenic role of each lncRNA involved in the molecular mechanism underlying PPROM, we have focused on investigating the metabolic pathways and their functions to explore what is the likely association and how they are possibly involved in the development of PPROM. Six groups, including up-regulation and down-regulation in the comparisons of A vs. B, A vs. C, and A vs. D, of pathways were analyzed. Our results showed that 22 pathways were characterized as up-regulated 7 down-regulated in A vs. C, 18 up-regulated and 15 down-regulated in A vs. D, and 33 up-regulated and 7 down-regulated in A vs. B. Functional analysis showed pathways of infection and inflammatory response, ECM-receptor interactions, apoptosis, actin cytoskeleton, and smooth muscle contraction are the major pathogenic mechanisms involved in the development of PPROM. Characterization of these pathways through identification of lncRNAs opened new avenues for further investigating the epigenomic mechanisms of lncRNAs in PPROM as well as PTB.
早产（PTB）是指妊娠 37 周前分娩（GW）。大约三分之一的 PTB 是由于早产胎膜早破（PPROM）引起的。迄今为止，PPROM 的发病机制尚不清楚。在这里，我们研究了 PPROM 胎盘长链非编码 RNA（lncRNA）的差异表达及其可能参与导致 PPROM 的致病途径。通过微阵列从 PPROM（A 组）胎盘中鉴定了总共 1954、776 和 1050 个 lncRNA，分别与足月产（FTB）（B 组）、PTB（C 组）和足月胎膜早破（PROM）（D 组）进行了比较。我们没有研究与 PPROM 发病机制相关的每个 lncRNA 的个体致病作用，而是专注于研究代谢途径及其功能，以探讨可能的关联以及它们如何可能参与 PPROM 的发生。分析了包括 A 与 B、A 与 C 和 A 与 D 比较中的上调和下调在内的 6 个组的途径。我们的结果表明，22 条途径在 A 与 C、A 与 D 和 A 与 B 的比较中被表征为上调 7 条下调，在 A 与 C 中 18 条上调和 15 条下调，在 A 与 D 中 33 条上调和 7 条下调。功能分析表明，感染和炎症反应、ECM-受体相互作用、细胞凋亡、肌动蛋白细胞骨架和平滑肌收缩等途径是 PPROM 发病的主要机制。通过鉴定 lncRNA 对这些途径的特征描述为进一步研究 lncRNA 在 PPROM 以及 PTB 中的表观基因组机制开辟了新途径。
