Journal
KIDNEY INTERNATIONAL
Volume 80, Issue 9, Pages 959-969Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ki.2011.250
Keywords
Akt; angiotensin II; apoptosis; peroxiredoxin 2; podocyte; reactive oxygen species
Categories
Funding
- Deutsche Forschungsgemeinschaft (DFG) [Pa 483/16-1]
Ask authors/readers for more resources
Podocytes have a significant role in establishing selective permeability of the glomerular filtration barrier. Sustained renin-angiotensin-aldosterone system activation is crucial to the pathogenesis of podocyte injury, but the mechanisms by which angiotensin II modulates podocyte survival due to physiological or injurious stimuli remain unclear. Here, we used proteomic analysis to find new mediators of angiotensin II-induced podocyte injury. Antioxidant protein peroxiredoxin 2 expression was decreased in cultured podocytes stimulated with angiotensin II. Peroxiredoxin 2 was found to be expressed in podocytes in vivo, and its expression was decreased in the glomeruli of rats transgenic for angiotensin II type 1 receptors in a podocyte-specific manner, or in rats infused with angiotensin II. Downregulation of peroxiredoxin 2 in podocytes resulted in increased reactive oxygen species release, protein overoxidation, and inhibition of the Akt pathway. Both treatment with angiotensin II and downregulation of peroxiredoxin 2 expression led to apoptosis of podocytes. Thus, peroxiredoxin 2 is an important modulator of angiotensin II-induced podocyte injury. Kidney International (2011) 80, 959-969; doi:10.1038/ki.2011.250; published online 3 August 2011
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available