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ISRN Endocrinology
Volume 2012 (2012), Article ID 549875, 6 pages
doi:10.5402/2012/549875
miR-320 Regulates Glucose-Induced Gene Expression in Diabetes
1Department of Pathology, Western University, London, ON, N6A 5C1, Canada
2London Health Science Centre, 339 Windermere Road, London, ON, N6A 5A5, Canada
Received 18 April 2012; Accepted 22 June 2012
Academic Editors: C. Bizzarri, J. Mittag, and H. Tamemoto
Copyright © 2012 Biao Feng and Subrata Chakrabarti. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
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.