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长链非编码 RNA TUG1 通过 novel regulatory mechanism network 介导导致子痫前期螺旋动脉重塑损伤的 novel 调控机制网络。

A novel regulatory mechanism network mediated by lncRNA TUG1 that induces the impairment of spiral artery remodeling in preeclampsia.

机构信息

Department of Obstetrics and Gynecology, First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, Jiangsu Province, P.R. China.

Department of Obstetrics and Gynecology, Women's Hospital of Nanjing Medical University, Nanjing Maternity and Child Health Care Hospital, 123 Tianfeixiang, Mochou Road, Qinhuai District, Nanjing 210004, China.

出版信息

Mol Ther. 2022 Apr 6;30(4):1692-1705. doi: 10.1016/j.ymthe.2022.01.043. Epub 2022 Feb 4.

DOI:10.1016/j.ymthe.2022.01.043
PMID:35124178
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9077368/
Abstract

Preeclampsia (PE) is associated with maternal and fetal perinatal morbidity and mortality, which brings tremendous suffering and imposes an economic burden worldwide. The failure of uterine spiral artery remodeling may be related to the abnormal function of trophoblasts and lead to the occurrence and progression of PE. Aberrant expression of long non-coding RNAs (lncRNAs) is involved in the failure of uterine spiral artery remodeling. However, the regulation of lncRNA expression in PE is poorly characterized. Here, we reported that hypoxia-induced microRNA (miR)-218 inhibited the expression of lncRNA TUG1 by targeting FOXP1. Further RNA sequencing and mechanism analysis revealed that silencing of TUG1 increased the expression of DNA demethylase TET3 and proliferation-related DUSP family, including DUSP2, DUSP4, and DUSP5, via binding to SUV39H1 in the nucleus. Moreover, TUG1 modulated the DUSP family in vitro through a TET3-mediated epigenetic mechanism. Taken together, our results unmask a new regulatory network mediated by TUG1 as an essential determinant of the pathogenesis of PE, which regulates cell growth and possibly the occurrence and development of other diseases.

摘要

子痫前期 (PE) 与母婴围产期发病率和死亡率有关，给全球带来了巨大的痛苦和经济负担。子宫螺旋动脉重塑的失败可能与滋养细胞的异常功能有关，并导致 PE 的发生和进展。长链非编码 RNA (lncRNA) 的异常表达参与了子宫螺旋动脉重塑的失败。然而，PE 中 lncRNA 表达的调控特征很差。在这里，我们报道了缺氧诱导的 microRNA (miR)-218 通过靶向 FOXP1 抑制 lncRNA TUG1 的表达。进一步的 RNA 测序和机制分析表明，沉默 TUG1 通过与核内 SUV39H1 结合，增加了 DNA 去甲基化酶 TET3 和增殖相关的 DUSP 家族（包括 DUSP2、DUSP4 和 DUSP5）的表达。此外，TUG1 通过 TET3 介导的表观遗传机制在体外调节 DUSP 家族。总之，我们的研究结果揭示了一个由 TUG1 介导的新的调节网络，作为 PE 发病机制的一个重要决定因素，调节细胞生长，并可能调节其他疾病的发生和发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/101b/9077368/45d012475185/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/101b/9077368/b32d2c746edd/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/101b/9077368/3edd82db06af/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/101b/9077368/5613df24ab78/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/101b/9077368/e2f2048f2078/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/101b/9077368/b90aed5cbfc1/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/101b/9077368/626804524c33/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/101b/9077368/9d17acab9512/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/101b/9077368/45d012475185/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/101b/9077368/b32d2c746edd/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/101b/9077368/3edd82db06af/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/101b/9077368/5613df24ab78/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/101b/9077368/e2f2048f2078/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/101b/9077368/b90aed5cbfc1/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/101b/9077368/626804524c33/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/101b/9077368/9d17acab9512/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/101b/9077368/45d012475185/gr7.jpg

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