Abstract:
:Due to limited treatment options, pre-eclampsia (PE) is associated with fetal perinatal and maternal morbidity and mortality. During the causes of PE, failure of uterine spiral artery remodeling which might be related to functioning abnormally of trophoblast cells, result in the occurrence and progression of PE. Recently, abnormal expression of long non-coding RNAs (lncRNAs), as imperative regulators involved in human diseases progression (included PE), which has been indicated by increasing evidence. In this research, we found that TUG1, a lncRNA, was markedly reduced in placental samples from patients with PE. Loss-function assays indicated that knockdown TUG1 significantly affected cell proliferation, apoptosis, migration and network formation in vitro. RNA-seq revealed that TUG1 could affect abundant genes, and then explore the function and regulatory mechanism of TUG1 in trophoblast cells. Furthermore, RNA immunoprecipitation and chromatin immunoprecipitation assays validated that TUG1 can epigenetically inhibit the level of RND3 through binding to EZH2, thus promoting PE development. Therefore, via illuminating the TUG1 mechanisms underlying PE development and progression, our findings might furnish a prospective therapeutic strategy for PE intervention.
journal_name
Cell Death Disjournal_title
Cell death & diseaseauthors
Xu Y,Ge Z,Zhang E,Zuo Q,Huang S,Yang N,Wu D,Zhang Y,Chen Y,Xu H,Huang H,Jiang Z,Sun Ldoi
10.1038/cddis.2017.503subject
Has Abstractpub_date
2017-10-12 00:00:00pages
e3104issue
10issn
2041-4889pii
cddis2017503journal_volume
8pub_type
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