Abstract
Long non-coding RNA MEG3 has been reported to implicate in the progression of several cancers. Nevertheless, few studies have focused on the role of MEG3 in the development of diabetic nephropathy. Here, we demonstrated MEG3 was differently expressed by > 4 fold and was elevated significantly using lncRNA microarray in DN patient serum. Besides, MEG3 knockdown alleviated proliferation, fibrosis and induced apoptosis of mesangial cells under high glucose condition. Furthermore, bioinformatics predictions showed that MEG3 is a direct target of miR-145. In the vivo experiment, we found MEG3 silencing decreased the laboratory indicators and fibrosis-related protein secretion in db/db mice. Altogether, our study suggests MEG3 may play as an important role in progression of diabetic nephropathy, contributing to a novel understanding of pathogenesis and underlying therapeutic strategies for diabetic nephropathy.