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产前暴露于 BP-3 与先天性巨结肠病的关系。

The relationship between prenatal exposure to BP-3 and Hirschsprung's disease.

机构信息

State Key Laboratory of Reproductive Medicine, Institute of Toxicology, Nanjing Medical University, Nanjing 211166, China; Key Laboratory of Modern Toxicology of Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing 211166, China.

State Key Laboratory of Reproductive Medicine, Institute of Toxicology, Nanjing Medical University, Nanjing 211166, China; Department of Pediatric Surgery, Nanjing Children's Hospital Affiliated Nanjing Medical University, Nanjing 210008, China.

出版信息

Chemosphere. 2016 Feb;144:1091-7. doi: 10.1016/j.chemosphere.2015.09.019. Epub 2015 Oct 23.

Abstract

Hirschsprung's disease (HSCR) is neonatal intestinal abnormality which derived from the faliure of enteric neural crest cells migration to hindgut during embryogenesis from 5 to 12 weeks. Currenly, the knowledge of environmental factors contributing to HSCR is still scarce. Benzophenone-3 (BP-3) is one of the most widely used UV filters, and has weak estrogen and strong anti-androgenic effects. In order to examine the effect of maternal BP-3 exposure on development of offspring and explore the potential mechanism, we conducted case and control study and in vitro study. In this work, BP-3 concertrations in maternal urine was detected by ultra-high performance liquid chromatography. Besides, we investigated the cytotoxicity and receptor tyrosine kinase (RET) expression in cells exposed to BP-3. The results showed that maternal BP-3 exposure was associated with offspring's HSCR in the population as well as inhibited migration of 293T and SH-SY5Y cells. What's more, we discovered dose-response relationship between RET expression and BP-3 exposure dose, and miR-218 and some other genes involved in SLIT2/ROBO1-miR-218-RET/PLAG1 pathway were also related to BP-3 exposure. Therefore, we deduced that BP-3 influenced cell migration via SLIT2/ROBO1-miR-218-RET/PLAG1 pathway. Our study firstly revealed the relationship between maternal BP-3 exposure and HSCR as well as its potential mechanism.

摘要

先天性巨结肠(HSCR)是一种新生儿肠道异常,它是由于胚胎发育过程中(第 5 周到第 12 周)肠神经嵴细胞向中肠迁移失败而导致的。目前,关于导致 HSCR 的环境因素的知识仍然匮乏。二苯甲酮-3(BP-3)是最广泛使用的紫外线滤光剂之一,具有较弱的雌激素和较强的抗雄激素作用。为了研究母体 BP-3 暴露对后代发育的影响并探讨其潜在机制,我们进行了病例对照研究和体外研究。在这项工作中,通过超高效液相色谱法检测了母体尿液中的 BP-3 浓度。此外,我们还研究了 BP-3 暴露对细胞的细胞毒性和受体酪氨酸激酶(RET)表达的影响。结果表明,母体 BP-3 暴露与人群中后代的 HSCR 有关,并抑制了 293T 和 SH-SY5Y 细胞的迁移。此外,我们发现 RET 表达与 BP-3 暴露剂量之间存在剂量反应关系,并且 SLIT2/ROBO1-miR-218-RET/PLAG1 通路中的 miR-218 和其他一些基因也与 BP-3 暴露有关。因此,我们推断 BP-3 通过 SLIT2/ROBO1-miR-218-RET/PLAG1 通路影响细胞迁移。我们的研究首次揭示了母体 BP-3 暴露与 HSCR 之间的关系及其潜在机制。

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