title: Inflammatory gene expression in OVE26 diabetic kidney during the development of nephropathy.
abstract: OBJECTIVE
  To define renal gene expression during the development of severe albuminuria in OVE26 diabetic mice.
  
  
  METHODS
  Kidney microarray analysis was performed at 2, 4 and 8 months. Data were validated by RT-PCR, in situ hybridization and immunohistochemistry.
  
  
  RESULTS
  Gene expression differences between control and diabetic mice increased 10-fold from 2 to 8 months. This change was most obvious for inflammatory genes. Three inflammatory genes, complement C3, VCAM1 and CD44 were upregulated more than 4-fold. Inflammatory gene expression correlated with albuminuria and C3 and CD44 increased in tubules that accumulated albumin. VCAM1 was induced in different tubules that were neither dilated nor accumulated albumin. Six of 8 genes previously reported to be markers of human advanced diabetic nephropathy and the NF-κB_IFN_x promoter module were elevated in the oldest diabetic mice. Vitamin D inhibits diabetic renal inflammation. Vitamin D and mRNA for vitamin D synthetic enzyme CYP2B1 were elevated in kidneys of young OVE26 mice.
  
  
  CONCLUSIONS
  OVE26 mice induce inflammatory genes consistent with advanced renal disease, associated with severe albuminuria and to a greater extent than reported in other diabetic models. They provide an excellent model of diabetic nephropathy to assess the effect of induction of inflammatory proteins.
authors: Department of Pharmacology and Toxicology, University of Louisville, Louisville, KY, USA.
authors: Lu
authors: L
authors: Yang
authors: Suzana
authors: S
authors: Brozovic
authors: Jianxiang
authors: J
authors: Xu
authors: Yunshi
authors: Y
authors: Long
authors: Patricia M
authors: PM
authors: Kralik
authors: Sabine
authors: S
authors: Waigel
authors: Wolfgang
authors: W
authors: Zacharias
authors: Shirong
authors: S
authors: Zheng
authors: Paul N
authors: PN
authors: Epstein