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miR-19a和miR-20a与活化的人外周血单个核细胞中组织因子表达的关系

miR-19a and miR-20a and Tissue Factor Expression in Activated Human Peripheral Blood Mononuclear Cells.

作者信息

Balia Cristina, Giordano Mirella, Scalise Valentina, Neri Tommaso, Fontanini Gabriella, Basolo Fulvio, Celi Alessandro, Pedrinelli Roberto

机构信息

Dipartimento di Patologia Chirurgica, Medica, Molecolare e dell'Area Critica, Università di Pisa, Pisa, Italy.

出版信息

Thrombosis. 2017;2017:1076397. doi: 10.1155/2017/1076397. Epub 2017 Oct 30.

Abstract

BACKGROUND AND AIMS

To investigate the behaviour of miR-19a and miR-20a, two microRNAs involved in posttranscriptional modulation of TF expression in peripheral blood mononuclear cells (PBMCs) exposed to high glucose (HG) and lipopolysaccharide (LPS), and to evaluate the involvement of angiotensin II in that process.

METHODS

TF Procoagulant Activity (PCA, one-stage clotting assay), antigen (Ag, ELISA), and miR-19a and miR-20a levels (specific TaqMan® MicroRNA Assays) were evaluated in PBMCs exposed to high glucose (HG, 50 mM), LPS (100 ng/mL), and Olmesartan (OLM, 10 M), an angiotensin II type 1 receptor antagonist.

RESULTS

HG increased TF expression and decreased both miRs as compared to control glucose conditions (11.1 mM). In HG-activated PBMCs, LPS stimulated TF expression and downregulated miR-20a, an effect reverted by OLM (10 M); miR-19a expression was unchanged by LPS in both CG and HG conditions.

CONCLUSIONS

miR-19a and miR-20a are inhibited by inflammatory stimuli active on TF expression and their response differs by the stimulus under investigation; angiotensin II may participate in that mechanism.

摘要

背景与目的

研究参与外周血单核细胞(PBMCs)中组织因子(TF)表达转录后调控的两种微小RNA(miR - 19a和miR - 20a)在暴露于高糖(HG)和脂多糖(LPS)时的行为,并评估血管紧张素II在此过程中的作用。

方法

在暴露于高糖(HG,50 mM)、脂多糖(LPS,100 ng/mL)和奥美沙坦(OLM,10 μM,一种血管紧张素II 1型受体拮抗剂)的PBMCs中,评估TF促凝活性(PCA,一期凝血试验)、抗原(Ag,ELISA)以及miR - 19a和miR - 20a水平(特异性TaqMan®微小RNA检测)。

结果

与对照葡萄糖条件(11.1 mM)相比,HG增加了TF表达并降低了两种miR的水平。在HG激活的PBMCs中,LPS刺激TF表达并下调miR - 20a,该效应被OLM(10 μM)逆转;在对照葡萄糖和HG条件下,LPS均未改变miR - 19a的表达。

结论

miR - 19a和miR - 20a受到对TF表达有活性的炎症刺激的抑制,并且它们对所研究刺激的反应有所不同;血管紧张素II可能参与该机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b2f/5682915/e21176264bf9/THROMBOSIS2017-1076397.001.jpg

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