A possible role of aryl hydrocarbon receptor in spontaneous preterm birth.
A possible role of aryl hydrocarbon receptor in spontaneous preterm birth.
复制标题
芳基烃受体在自发性早产中的可能作用。
DOI：
10.1016/j.mehy.2015.02.001
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发表时间：
2015-05
影响因子：
4.7
通讯作者：
Zheng, Jing
中科院分区：
文献类型：
--
作者：
Li, Yan;Wang, Kai;Zou, Qing-Yun;Zhou, Chi;Magness, Ronald R.;Zheng, Jing
早产（PTB）定义为妊娠37周之前出生，是新生儿死亡和发病的主要原因。迄今为止，自发性PTB（sPTB）的病因仍不清楚;然而，宫内细菌感染诱导的炎症被认为是主要的触发因素之一。芳烃受体（Aryl hydrocarbon receptor，AhR）是一种配体依赖性转录因子。一旦激活，AhR信号传导介导许多生物过程。AhR在人胎盘中大量表达，主要在滋养层和几种胎儿器官和组织中。AhR信号的激活可以通过促进胎盘和胎膜产生促炎细胞因子来调节炎症反应。这些细胞因子可以增强人滋养层和羊膜上皮中环氧合酶-2（COX 2）的表达和/或活性，这又刺激了前列腺素（PGs;例如，PGE 2和PGF 2 α）。鉴于在人类中发现了许多天然和内源性AhR配体，我们假设在胎盘和胎膜中具有高AhR表达的患者亚组中，反复暴露于这些AhR配体使AhR过度活化，诱导细胞因子/COX 2/PGs通路的过度活化，导致子宫肌层收缩，最终导致sPTB。我们进一步假设该AhR途径的过度活化可以直接或与细菌感染协同诱导sPTB。这一假设的证明可能提供一种新的机制，潜在的sPTB。
Preterm birth (PTB) is defined as birth before 37 weeks of gestation and is a leading cause of neonatal mortality and morbidity. To date, the etiology of spontaneous PTB (sPTB) remains unclear; however, intrauterine bacterial infection-induced inflammation is considered to be one of the major triggers. Aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor. Upon activation, AhR signaling mediates many biological processes. AhR is abundantly expressed in human placentas, primarily in trophoblasts, and several fetal organs and tissues. The activation of AhR signaling can modulate inflammatory responses via promoting production of pro-inflammatory cytokines by the placenta and fetal membranes. These cytokines could enhance expression and/or activity of cyclooxygenase-2 (COX2) in human trophoblasts and amniotic epithelia, which in turn stimulate synthesis and release of prostaglandins (PGs; e.g., PGE2 and PGF2α). Given the discovery of a number of natural and endogenous AhR ligands in human, we hypothesize that in a subset of patients with high AhR expression in placentas and fetal membranes, repeated exposure to these AhR ligands hyperactivates AhR, inducing hyperactivation of the cytokines/COX2/PGs pathway, resulting in myometrial contractions, ultimately leading to sPTB. We further hypothesize that hyperactivation of this AhR pathway can induce sPTB either directly or in synergy with the bacterial infection. Proof of this hypothesis may provide a novel mechanism underlying sPTB.
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影响因子：
3.5
作者：
Paganga, G;RiceEvans, CA
通讯作者：
RiceEvans, CA
影响因子：
3.6
作者：
Dominguez-Lopez, Pablo;Diaz-Cueto, Laura;Arechavaleta-Velasco, Fabian
通讯作者：
Arechavaleta-Velasco, Fabian
DOI：
10.1016/s0090-6980(96)00088-3
发表时间：
1996-10-01
期刊：
PROSTAGLANDINS
影响因子：
--
作者：
Fuentes, A;Spaziani, EP;OBrien, WF
通讯作者：
OBrien, WF
影响因子：
12.8
作者：
Cheon, HyeonJoo;Woo, Young-Seok;Sohn, Jeongwon
通讯作者：
Sohn, Jeongwon
影响因子：
3.9
作者：
Hao, Kehong;Zhou, Qian;Duan, Tony
通讯作者：
Duan, Tony