Long Non-Coding RNA Nuclear Paraspeckle Assembly Transcript 1: A Regulator of Trophoblast Cells in the Progression of Gestational Diabetes Mellitus

IF 0.9 4区 材料科学 Science of Advanced Materials Pub Date : 2023-05-01 DOI:10.1166/sam.2023.4486
Wushan Li, Xiaojuan Wang, Dongdong Hao
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Abstract

The potential function of NEAT1 in the progression of Gestational diabetes mellitus (GDM) and the molecular mechanisms are explored. NEAT1 levels in multiple types of cell lines and placental tissues collected from healthy, GDM and preeclampsia pregnancies were detected by quantitative real-time polymerase chain reaction (qRT-PCR). After intervening NEAT1 level in HTR-8/SVneo cells, proliferative, migratory and apoptotic potentials were examined by cell counting kit-8 (CCK-8), 5-Ethynyl-2′-deoxyuridine (EdU), transwell assay and flow cytometry. The regulatory effect of NEAT1 on the transcriptional activity of NSD1 was predicted by bioinformatic analysis and further confirmed by dual-luciferase reporter assay. In addition, histone modifications of NEAT1 on NSD1 transcription were examined by chromatin immunoprecipitation (ChIP). NEAT1 was upregulated in placental tissues collected from GDM patients. Overexpression of NEAT1 stimulated proliferative and migratory potentials, but inhibited apoptosis in HTR-8/SVneo cells. Knockdown of NEAT1 had the opposite outcomes. NEAT1 was able to regulate the transcriptional activity of NSD1 through histone modifications on H3K27Me3 and H3K27Cro. NEAT1 is upregulated in GDM cases, which triggers proliferative and migratory potentials in trophoblast cells mainly through regulating transcriptional activity of NSD1 via histone modification.
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长非编码RNA核旁装配转录物1:妊娠期糖尿病进展中滋养层细胞的调节因子
探讨NEAT1在妊娠期糖尿病(GDM)发展中的潜在功能及其分子机制。采用实时定量聚合酶链反应(qRT-PCR)技术检测健康妊娠、GDM妊娠和子痫前期妊娠的多种细胞系和胎盘组织中NEAT1水平。干预HTR-8/SVneo细胞NEAT1水平后,采用细胞计数试剂盒-8 (CCK-8)、5-乙基-2′-脱氧尿苷(EdU)、transwell实验和流式细胞术检测细胞增殖、迁移和凋亡电位。通过生物信息学分析预测NEAT1对NSD1转录活性的调控作用,并通过双荧光素酶报告基因实验进一步证实。此外,通过染色质免疫沉淀(ChIP)检测NEAT1对NSD1转录的组蛋白修饰。NEAT1在GDM患者胎盘组织中表达上调。过表达NEAT1刺激HTR-8/SVneo细胞的增殖和迁移潜能,但抑制细胞凋亡。NEAT1基因敲低则有相反的结果。NEAT1能够通过H3K27Me3和H3K27Cro上的组蛋白修饰来调节NSD1的转录活性。NEAT1在GDM病例中表达上调,主要通过组蛋白修饰调节NSD1的转录活性,触发滋养细胞的增殖和迁移潜能。
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来源期刊
Science of Advanced Materials
Science of Advanced Materials NANOSCIENCE & NANOTECHNOLOGY-MATERIALS SCIENCE, MULTIDISCIPLINARY
自引率
11.10%
发文量
98
审稿时长
4.4 months
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