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Journal of Diabetes Research
Volume 2013 (2013), Article ID 979702, 8 pages
Research Article

Notch Signaling Molecules Activate TGF-β in Rat Mesangial Cells under High Glucose Conditions

1Department of Endocrinology, The Affiliated Hospital of Luzhou Medical College, Luzhou, Sichuan, China
2Department of Endocrinology, The People's Hospital of Yongchuan, Yongchuan, Chongqing, China
3Department of Endocrinology, The First Hospital of Yibin, Yibin, Sichuan, China

Received 27 November 2012; Revised 17 March 2013; Accepted 31 March 2013

Academic Editor: Aimin Xu

Copyright © 2013 Li Liu et al. 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.


The involvement of the Notch signaling pathway in the cellular differentiation of the mammalian kidney is established. Recently, the dysregulation of Notch signaling molecules has been identified in acute and chronic renal injuries, fibrosis models, and diabetic kidney biopsies. The canonical Notch ligand , Jagged1, is upregulated in a transforming growth factor-beta- (TGF-β-) dependent manner during chronic kidney disease. TGF-β, a central mediator of renal fibrosis, also is a major contributor to the development of diabetic nephropathy. To explore the roles and possible mechanisms of Notch signaling molecules in the pathogenesis of diabetic nephropathy, we exposed cultured rat mesangial cells to a γ-secretase inhibitor (DAPT) or high glucose and measured the expression of Notch signaling molecules and the fibrosis index. Notch pathway-related molecules, TGF-β, and fibronectin increased with exposure to high glucose and decreased with DAPT treatment. Our results suggest that the Notch signaling pathway may precipitate diabetic nephropathy via TGF-β activation.