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Dysregulation of miR-637 is involved in the development of retinopathy in hypertension patients and serves a regulatory role in retinol endothelial cell proliferation
Ophthalmic Research ( IF 2.0 ) Pub Date : 2021-02-02 , DOI: 10.1159/000514915
Weiguang Yang 1 , Manxia Su 2 , Yanli Yu 2 , Qingxin Fang 2 , Jihong Zhang 3 , Jihong Zhang 1, 2, 3
Affiliation  

Background: MicroRNAs (miRNAs) play an important role in the proliferation and migration of retinal endothelial cells in patients with hypertension and hypertensive retinopathy (HR). This study aimed to investigate the clinical value of miR-637 in HR and its role in retinal endothelial cell proliferation and migration. Methods: A total of 126 subjects were recruited for the study, including 42 patients with hypertension (male/female 25/17), 42 healthy individuals (male/female 20/22), and 42 cases with HR (male/female 20/22). Except SBP and DBP, there was no significant difference in other indexes among the three groups. qRT-PCR was used to detect the expression of miR-637. The receiver operating curve (ROC) was used for diagnosis value analysis. Logistic regression analysis was used to evaluate the relationship between miR-637 and HR. CCK-8 and Transwell were used to detect the effect of miR-637 on the proliferation and migration of HUVECs. Results: Compared with hypertensive patients, HR patients had the lowest expression of miR-637. The area under the curve (AUC) of miR-637 detected by the ROC curve method is 0.892, which has the ability to distinguish hypertension and HR patients. Logistic regression analysis showed that miR-637 was an independent influence factor in HR. Cell experiment results showed that overexpression of miR-637 significantly inhibited cell proliferation and migration, while downregulation of miR-637 had the opposite effect. Luciferase analysis showed that STAT3 was the target gene of miR-637. Conclusion: Our data indicate that miR-637 is a potential non-invasive marker for patients with HR. The action of miR-637 on STAT3 may inhibit the proliferation and migration of retinal endothelial cells, providing a possible target for the treatment of HR.


中文翻译:


miR-637 失调参与高血压患者视网膜病变的发生,并在视黄醇内皮细胞增殖中发挥调节作用



背景:微小RNA(miRNA)在高血压和高血压性视网膜病变(HR)患者视网膜内皮细胞的增殖和迁移中发挥重要作用。本研究旨在探讨miR-637在HR中的临床价值及其在视网膜内皮细胞增殖和迁移中的作用。方法:共纳入126名受试者,其中高血压患者42例(男/女25/17),健康人42例(男/女20/22),HR患者42例(男/女20/22)。 22)。除收缩压和舒张压外,三组间其他指标均无显着性差异。采用qRT-PCR检测miR-637的表达。采用受试者工作曲线(ROC)进行诊断价值分析。使用Logistic回归分析评估miR-637与HR之间的关系。采用CCK-8和Transwell检测miR-637对HUVEC增殖和迁移的影响。结果:与高血压患者相比,HR患者miR-637表达最低。 ROC曲线法检测的miR-637曲线下面积(AUC)为0.892,具有区分高血压和HR患者的能力。 Logistic回归分析显示miR-637是HR的独立影响因素。细胞实验结果表明,miR-637的过表达显着抑制细胞增殖和迁移,而下调miR-637则具有相反的效果。荧光素酶分析表明STAT3是miR-637的靶基因。结论:我们的数据表明 miR-637 是 HR 患者的潜在非侵入性标志物。 miR-637对STAT3的作用可能抑制视网膜内皮细胞的增殖和迁移,为HR的治疗提供可能的靶点。
更新日期:2021-02-02
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