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LncRNA CASC2通过海绵式miR-152-3pp调解下肢深静脉血栓形成

Shuping Wang¹, Hongyu Yang¹, Fei Wang¹

¹Department of Clinical Laboratory, Affiliated Hospital of PanZhiHua University, No.27 Taoyuan Street, Bingcaogang, East District, Panzhihua City, 617000, Sichuan Province, China.

Journal of thrombosis and thrombolysis

|July 2, 2025

概括

长非编码RNACASC2在深静脉血栓症 (DVT) 中被下调,并通过准miR-152-3p来调节其形成. 这个轴在DVT的发病过程中至关重要.

科学领域:

分子生物学分子生物学
遗传学是一个遗传学.
血管生物学血管生物学

背景情况:

深静脉血栓症 (DVT) 是一种常见的血管疾病,发生率很高.
研究DVT的调控机制对于了解其病变发生至关重要.

研究的目的:

阐明长非编码RNA (lncRNA) CASC2 / miR-152-3p轴在DVT调节中的作用.
确定涉及CASC2和miR-152-3p的DVT形成的分子机制.

主要方法:

在使用RT-qPCR的DVT患者和对照组中量化CASC2和miR-152-3p水平.
评估人类静脉内皮细胞 (HUVEC) 的活力,迁移和亡.
通过ELISA测量炎症标记物和粘附分子.
使用双露西法酶记者试验验证CASC2和miR-152-3p之间的相互作用.
使用GO和KEGG进行功能和通路丰富分析.

主要成果:

在DVT患者中,LncRNA CASC2显著下调,并与DVT发生相关.
过度表达CASC2增强了HUVEC的扩散和迁移,同时减少了亡和炎症.
CASC2直接向和负调节miR-152-3p,这抵消了CASC2的影响.
miR-152-3p目标基因参与TGF-β和PI3K-Akt信号通路.

结论:

lncRNA CASC2 / miR-152-3p轴是DVT病变发生的关键调节器.
这个轴的失调有助于深静脉血栓的发展.

关键词:

细胞功能细胞功能在LncRNA CASC2 中.下肢深静脉血栓形成的原因在 miR-152-3pp 中.

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