Tenascin-X in amniotic fluid and reproductive tissues of pregnancies complicated by infection and preterm prelabor rupture of membranes†.
Tenascin-X in amniotic fluid and reproductive tissues of pregnancies complicated by infection and preterm prelabor rupture of membranes†.
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妊娠期羊水和生殖组织中的腱蛋白-X 并发感染和早产胎膜破裂。
DOI：
10.1093/biolre/ioy216
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发表时间：
2019
影响因子：
3.6
通讯作者：
Buhimschi,IrinaA
中科院分区：
文献类型：
--
作者：
Rood,KaraM;Buhimschi,CatalinS;Zhao,Guomao;Oliver,EmilyA;Summerfield,Taryn;Bahtiyar,MertOzan;Buhimschi,IrinaA
早产前胎膜破裂（PPROM），可发生在羊膜内感染/炎症（IAI）之前或之后，是一种知之甚少的妊娠并发症。腱生蛋白-X（TNX）是一种结缔组织细胞外基质蛋白，调节胶原蛋白I，III和V的纤维形成。我们的目标是研究羊水（AF）中可溶性TNX（sTNX）的存在和水平以及妊娠合并PPROM和IAI的生殖组织中TNX的表达。我们前瞻性地招募了334名单胎妊娠的妇女，这些妇女在有或没有PPROM的情况下进行了临床指征的肺穿刺术，以进行遗传核型分析、肺成熟度检测或排除IAI。我们使用免疫学方法和qRT-PCR定量TNX在胎膜、子宫肌层、宫颈和胎盘中的表达。在妊娠结局正常的孕妇中，AF sTNX水平受GA调节，足月时水平较低。IAI显著上调AF sTNX水平，与膜状态无关。AF sTNX水平与胎膜tenascin XB（TNXB）mRNA水平呈负相关，IAI显著下调TNXB mRNA水平。免疫印迹法鉴定了AF和胎膜中的特征性sTNX-75和sTNX-140 kDa形式。胎膜、胎盘和子宫颈组成性表达TNX，羊膜中丰度最高。羊膜TNX丰富度在IAI中显著丧失。我们的研究结果表明，胎膜可能是AF sTNX的来源，其中蛋白质和mRNA的表达似乎显着影响独立于胎膜状态的炎症。更彻底地了解TNX的变化可能对了解自发性PPROM和潜在的治疗靶点有价值。
Preterm prelabor rupture of membranes (PPROM), which can precede or follow intra-amniotic infection/inflammation (IAI), is a poorly understood pregnancy complication. Tenascin-X (TNX) is a connective tissue extracellular matrix protein that regulates fibrillogenesis of collagens I, III, and V. Our goal was to investigate the presence and level of soluble TNX (sTNX) in amniotic fluid (AF) and TNX expression in reproductive tissues of pregnancies complicated by PPROM and IAI. We prospectively recruited 334 women pregnant with singletons who had a clinically indicated amniocentesis for genetic karyotyping, lung maturity testing, or rule-out IAI in the presence or absence of PPROM. We quantified TNX expression in fetal membranes, myometrium, cervix, and placenta using immunological methods and qRT-PCR. In pregnancies with normal outcomes, AF sTNX levels were GA-regulated with lower levels toward term. IAI significantly upregulated AF sTNX levels independent of membrane status. AF sTNX levels inversely correlated with fetal membranes tenascin XB (TNXB) mRNA level, which was significantly downregulated by IAI. Western blotting identified characteristic ∼75 and ∼140 kDa sTNX forms in both AF and fetal membranes. Fetal membranes, placenta, and cervix constitutively express TNX with the highest abundance in the amnion. Amnion TNX richness is significantly lost in the setting of IAI. Our results suggest that fetal membranes may be a source of AF sTNX whereby protein and mRNA expression seem to be significantly impacted by inflammation independent of fetal membrane status. A more thorough understanding of TNX changes may be valuable for understanding spontaneous PPROM and to potentially develop therapeutic targets.