利用纳米传感器原位检测 miR-93/VEGFR2 并抑制滋养细胞凋亡

IF 0.7 4区 材料科学 Q3 Materials Science
Yanru Zhou, Yimei Ji, Yan Cheng
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引用次数: 0

摘要

我们研究了复发性自然流产(RSA)的发病机制,并评估了滋肾育胎丸(PNKF)的治疗效果。我们使用了一种灵敏的 DNA 传感器来检测 miR-93 的表达和血管内皮生长因子受体 2(VEGFR2)。我们测试了 DNA 传感器的穿透能力和理化性质,发现该传感器具有较高的穿透能力和良好的稳定性,在不同的反应温度和介质中能有效地检测 miR-93 和 VEGFR2,且荧光信号相似。该传感器能检测到 RSA 患者体内较高的 miR-93 表达、凋亡增加以及 VEGFR2 的负调控。用 PNKF 处理从 RSA 患者体内收集的滋养层细胞,能显著抑制滋养层细胞凋亡,并通过降低 miR-93 表达和促进 VEGFR2 表达来促进滋养层细胞增殖。总之,PNKF可通过抑制miR-93和促进VEGFR2的表达来改善滋养细胞的增殖和抑制其凋亡。此外,miR-93/VEGFR2 传感器还具有高灵敏度,有望应用于临床实践。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
In situ detection of miR-93/VEGFR2 by nanosensor and inhibition of trophoblast apoptosis
We investigated the pathogenesis of recurrent spontaneous abortion (RSA) and evaluated the therapeutic effect of Pill Nourishing Kidney and Fetus (PNKF). A sensitive DNA sensor was used to detect miR-93 expression and vascular endothelial growth factor receptor 2 (VEGFR2). We testing the penetration capacity and physicochemical properties of the DNA sensor and found that the sensor had higher penetration and good stability and effectively detected miR-93 and VEGFR2 at different reaction temperatures and mediums with similar fluorescence signals. The sensor detected higher miR-93 expression, increased apoptosis, and negative regulation of VEGFR2 in patients with RSA. Treatment with PNKF of cultured trophoblast cells collected from patients with RSA were treated with PNKF significantly inhibited trophoblast cell apoptosis and promoted trophoblast cell proliferation by reducing miR-93 expression and promoting VEGFR2 expression. In conclusion, PNKF can improve the proliferation and inhibit apoptosis of trophoblast cells by suppressing miR-93 and promoting VEGFR2. Furthermore, the miR-93/VEGFR2 sensor demonstrated high sensitivity that has potential applications in clinical practice.
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来源期刊
Materials Express
Materials Express NANOSCIENCE & NANOTECHNOLOGY-MATERIALS SCIENCE, MULTIDISCIPLINARY
自引率
0.00%
发文量
69
审稿时长
>12 weeks
期刊介绍: Information not localized
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