Suppr超能文献

microRNA-155 调节重度子痫前期孕妇脐静脉内皮细胞中血管紧张素 II 型 1 受体的表达。

microRNA-155 regulates angiotensin II type 1 receptor expression in umbilical vein endothelial cells from severely pre-eclamptic pregnant women.

机构信息

Central Laboratory, International Peace Maternity and Child Health Hospital, Shanghai Jiaotong University, Shanghai 200030, P.R. China.

出版信息

Int J Mol Med. 2011 Mar;27(3):393-9. doi: 10.3892/ijmm.2011.598. Epub 2011 Jan 13.

Abstract

Angiotensin II is critical in pre-eclampsia pathogenesis. In addition, microRNA-155 regulates angiotensin II type 1 receptor expression. We have explored the function of microRNA-155 in pre-eclamptic pregnant women. Human umbilical vein endothelial cells were isolated and cultured from healthy puerperant women and pre-eclampsia patients. The cells were transfected with a mature microRNA-155 plasmid. The effect of microRNA-155 was assessed by Northern blotting, in situ hybridization, quantitative real-time PCR, immunofluorescent staining and Western blotting. In addition, activation of extracellular signal-regulated kinase 1/2 was assessed by co-immunoprecipitation and Western blotting. Severely pre-eclamptic pregnant women expressed less mature miR-155 compared to healthy pregnant women. In addition, angiotensin II type 1 receptor expression decreased substantially in healthy cells and miR-155-transfected cells compared to miR-155-mutant-transfected cells and cells from pre-eclamptic patients. Mature miR-155 reduced angiotensin II-induced extracellular signal-regulated kinase 1/2 activation. In conclusion, endogenous mature miR-155 expression may be an important contributor to the pathogenesis of severe pre-eclampsia.

摘要

血管紧张素 II 在子痫前期发病机制中起关键作用。此外,miRNA-155 调节血管紧张素 II 型 1 受体的表达。我们探讨了 miRNA-155 在子痫前期孕妇中的功能。从健康产妇和子痫前期患者中分离和培养人脐静脉内皮细胞。用成熟的 miRNA-155 质粒转染细胞。通过Northern 印迹、原位杂交、实时定量 PCR、免疫荧光染色和 Western blot 评估 miRNA-155 的作用。此外,通过共免疫沉淀和 Western blot 评估细胞外信号调节激酶 1/2 的激活。与健康孕妇相比,严重子痫前期孕妇表达的成熟 miR-155 较少。此外,与 miR-155 突变体转染细胞和来自子痫前期患者的细胞相比,血管紧张素 II 型 1 受体表达在健康细胞和 miR-155 转染细胞中显著降低。成熟的 miR-155 减少了血管紧张素 II 诱导的细胞外信号调节激酶 1/2 的激活。总之,内源性成熟 miR-155 的表达可能是严重子痫前期发病机制的重要因素。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验