DCTPP1通过AUF1调控人绒毛滋养细胞氧化应激稳态。

IF 7 2区 生物学 Q1 CELL BIOLOGY
Yajuan Lu, Xue Wu, Lei He, Peng Pan, Anqi Zhao, Tangli Kan, Yuting Chu, Jinglin Dong, Shuangkai Xu, Xiaofang Tan, Xiaoqing Yang
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引用次数: 0

摘要

胎盘滋养细胞功能障碍是导致漏产的主要原因之一。特定分子的表达和调控在这一复杂的过程中起着至关重要的作用。其中,人脱氧胞苷三磷酸焦磷酸酶1 (DCTPP1)作为关键酶,不仅参与核苷酸代谢,而且在维持基因组稳定性方面发挥着不可或缺的作用。为了更深入地研究DCTPP1在胎盘滋养细胞功能中的作用机制,我们使用了一株永生化的人妊娠早期上皮外滋养细胞系(HTR8/SVneo)作为功能研究的实验模型。DCTPP1表达的降低导致氧化应激的增加和细胞活力的降低,最终导致细胞凋亡。进一步分析发现DCTPP1与富au元素rna结合蛋白1 (AUF1)之间存在相互作用。AUF1的降低可诱导氧化应激失衡,导致HTR8/SVneo细胞凋亡。这些发现突出了DCTPP1作为一种潜在的生物标志物和治疗或预防MA的有效药物靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
DCTPP1 regulates oxidative stress homeostasis via AUF1 in human villous trophoblasts.

Placental trophoblast dysfunction is one of the main causes of missed abortion (MA). The expression and regulation of specific molecules play crucial roles in this complex process. Among these, human deoxycytidine triphosphate pyrophosphatase 1 (DCTPP1), a key enzyme, not only participates in nucleotide metabolism but also plays an indispensable role in maintaining genomic stability. To delve deeper into the mechanism of DCTPP1 in placental trophoblast cell function, we used an immortalized human first-trimester extravillous trophoblast cell line (HTR8/SVneo) as an experimental model for functional studies. A decrease in DCTPP1 expression leads to an increase in oxidative stress and decreased cell viability ultimately leading to apoptosis. Further analysis revealed an interaction between DCTPP1 and the AU-rich element RNA-binding protein 1 (AUF1). A decrease of AUF1 induced oxidative stress imbalance, leading to apoptosis in HTR8/SVneo cells. These findings highlight DCTPP1 as a potential biomarker and an effective drug target for the treatment or prevention of MA.

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来源期刊
Cell Death Discovery
Cell Death Discovery Biochemistry, Genetics and Molecular Biology-Cell Biology
CiteScore
8.30
自引率
1.40%
发文量
468
审稿时长
9 weeks
期刊介绍: Cell Death Discovery is a multidisciplinary, international, online-only, open access journal, dedicated to publishing research at the intersection of medicine with biochemistry, pharmacology, immunology, cell biology and cell death, provided it is scientifically sound. The unrestricted access to research findings in Cell Death Discovery will foster a dynamic and highly productive dialogue between basic scientists and clinicians, as well as researchers in industry with a focus on cancer, neurobiology and inflammation research. As an official journal of the Cell Death Differentiation Association (ADMC), Cell Death Discovery will build upon the success of Cell Death & Differentiation and Cell Death & Disease in publishing important peer-reviewed original research, timely reviews and editorial commentary. Cell Death Discovery is committed to increasing the reproducibility of research. To this end, in conjunction with its sister journals Cell Death & Differentiation and Cell Death & Disease, Cell Death Discovery provides a unique forum for scientists as well as clinicians and members of the pharmaceutical and biotechnical industry. It is committed to the rapid publication of high quality original papers that relate to these subjects, together with topical, usually solicited, reviews, editorial correspondence and occasional commentaries on controversial and scientifically informative issues.
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