Division of Maternal-Fetal Medicine and Perinatal Research, Department of Obstetrics and Gynecology, The University of Texas Medical Branch at Galveston, Galveston, Texas, United States of America.
PLoS One. 2012;7(2):e31136. doi: 10.1371/journal.pone.0031136. Epub 2012 Feb 13.
Rupture of the fetal membranes is a common harbinger of imminent labor and delivery. Telomere shortening is a surrogate for oxidative stress (OS) and senescence. Fetal leukocyte and placental membrane DNA telomere lengths were evaluated to determine their association with preterm prelabor rupture of the membranes (pPROM) or spontaneous preterm births with intact membranes (PTB), compared to term birth.
Telomere lengths were quantified in cord blood leukocytes (n = 133) from three major groups: 1) pPROM (n = 28), 2) PTB (n = 69) and 3) uncomplicated full term births (controls, n = 35), using real-time quantitative PCR. Placental membrane specimens (n = 18) were used to correlate fetal leukocyte and placental telomere lengths. Telomere length differences among the groups were analyzed by ANOVA. Pearson correlation coefficients determined relationships between leukocyte and placental membrane telomere lengths.
In pregnancies with intact membranes, fetal leukocyte telomere length was inversely proportional to gestational age. The mean telomere length decreased as gestation progressed, with the shortest at term. pPROM had telomere lengths (9962 ± 3124 bp) that were significantly shorter than gestational age-matched PTB (11546 ± 4348 bp, p = 0.04), but comparable to term births (9011 ± 2497 bp, p = 0.31). Secondary analyses revealed no effects of race (African American vs. Caucasian) or intraamniotic infection on telomere length. A strong Pearson's correlation was noted between fetal leukocyte and placental membrane telomere lengths (ρ = 0.77; p<0.01).
Fetal leukocyte telomere length is reduced in pPROM compared to PTB but is similar to term births. pPROM represents a placental membrane disease likely mediated by OS-induced senescence.
胎膜破裂是分娩即将开始的常见先兆。端粒缩短是氧化应激（OS）和衰老的替代指标。评估胎儿白细胞和胎盘膜 DNA 端粒长度，以确定它们与早产胎膜早破（pPROM）或无胎膜破裂的自发性早产（PTB）与足月分娩的关系。
使用实时定量 PCR 定量分析脐带血白细胞中的端粒长度（n = 133），分为三个主要组：1）pPROM（n = 28），2）PTB（n = 69）和 3）无并发症的足月分娩（对照组，n = 35）。使用胎盘膜标本（n = 18）来关联胎儿白细胞和胎盘端粒长度。通过方差分析分析组间端粒长度差异。Pearson 相关系数确定白细胞和胎盘膜端粒长度之间的关系。
在无胎膜破裂的妊娠中，胎儿白细胞端粒长度与胎龄呈反比。随着胎龄的进展，端粒长度逐渐缩短，足月时最短。pPROM 的端粒长度（9962 ± 3124 bp）明显短于胎龄匹配的 PTB（11546 ± 4348 bp，p = 0.04），但与足月分娩相当（9011 ± 2497 bp，p = 0.31）。次要分析显示种族（非裔美国人与白种人）或羊膜内感染对端粒长度没有影响。胎儿白细胞和胎盘膜端粒长度之间存在很强的 Pearson 相关关系（ρ = 0.77；p <0.01）。
与 PTB 相比，pPROM 中的胎儿白细胞端粒长度降低，但与足月分娩相似。pPROM 代表一种胎盘膜疾病，可能由 OS 诱导的衰老介导。
