miR-320调控糖尿病中葡萄糖诱导的基因表达。

ISRN endocrinology Pub Date : 2012-01-01 Epub Date: 2012-07-31 DOI:10.5402/2012/549875
Biao Feng, Subrata Chakrabarti
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引用次数: 86

摘要

mirna在多种生物过程中发挥重要作用。在这里,我们研究了miR-320在葡萄糖诱导的血管活性因子和细胞外基质(ECM)蛋白增强生产中的作用。高糖暴露降低了人脐静脉内皮细胞(HUVECs)中microRNA 320 (miR-320)的表达,但增加了内皮素1 (ET-1)、血管内皮生长因子(VEGF)和纤维连接蛋白(FN)的表达。转染miR-320模拟物可恢复高糖处理HUVECs中ET-1、VEGF和FN mRNA和蛋白的表达。此外,miR-320模拟转染降低了葡萄糖诱导的ERK1/2扩增产生。本研究数据表明,miR-320通过ERK 1/2负调控ET-1、VEGF和FN的表达。这种葡萄糖诱导的调节基因表达的新机制的发现可能为糖尿病并发症的治疗提供新的策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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miR-320 Regulates Glucose-Induced Gene Expression in Diabetes.

miRNAs play an important role in several biological processes. Here, we investigated miR-320 in glucose-induced augmented production of vasoactive factors and extracellular matrix (ECM) proteins. High glucose exposure decreased the expression of microRNA 320 (miR-320) but increased the expression of endothelin 1 (ET-1), vascular endothelial growth factor (VEGF), and fibronectin (FN) in human umbilical vein endothelial cells (HUVECs). Transfection of miR-320 mimics restored ET-1, VEGF and FN mRNA, and protein expression in HUVECs treated with high glucose. Furthermore, miR-320 mimic transfection reduced glucose-induced augmented production of ERK1/2. Data from this study indicates that miR-320 negatively regulates expression of ET-1, VEGF, and FN through ERK 1/2. Identification of such novel glucose-induced mechanism regulating gene expression may offer a new strategy for the treatment of diabetic complications.

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