Home
Deutsch
Advanced Search
Browse by ...
Publication overview
Contact persons
Help
DOI
PMC
 |
|
Open Access Green as soon as Postprint is submitted to ZB.
Modulation of glutathione peroxidase activity by age-dependent carbonylation in glomeruli of diabetic mice.
J. Diab. Complic. 32, 130-138 (2018)
Aims: Low levels of reactive oxygen species and resulting oxidative protein modifications may play a beneficial role in cellular function under stress conditions. Here we studied the influence of age-dependent protein carbonylation on expression and activity of the anti-oxidative selenoenzyme glutathione peroxidase(GPx) in insulin-deficient Ins2(Akita) mice and type 2 diabetic obese db/db mice in context of diabetic nephropathy. Methods: Protein carbonylation, GPx expression and activity were examined in kidney tissue and lysates by common histological and protein biochemical methods. Results: In kidneys of Ins2(Akita) mice, carbonylated proteins, GPx-1 and GPx-4 expression were mainly detected in podocytes and mesangial cells. GPx activity was increased in kidney cortex homogenates of these mice. Remarkably, young animals did not show a concomitant increase in GPx expression but enhanced GPx carbonylation. No carbonylation-dependent modification of GPx activity was detected in db/db mice. In cultured podocytes hyperglycemia induced an increase in GPx expression but had no effect on activity or carbonylation. In kidney tissue sections of type 1 or type 2 diabetes patients, GPx-1 and GPx-4 expression but not overall protein carbonylation was significantly decreased. Conclusions: These results indicate the existence of a threshold for beneficial carbonylation-dependent redox signaling during the progression of diabetic nephropathy. (C) 2017 Elsevier Inc. All rights reserved.
Altmetric
Additional Metrics?
Edit extra informations
Login
Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Diabetic Nephropathy ; Protein Carbonylation ; Reactive Oxygen Species ; Hyperglycemia ; Glutathione Peroxidase ; Podocytes; Oxidative Stress; Protein Carbonylation; Renal-disease; Nephropathy; Kidney; Expression; Podocyte; System; Target
ISSN (print) / ISBN
1056-8727
e-ISSN
1056-8727
Quellenangaben
Volume: 32,
Issue: 2,
Pages: 130-138
Publisher
Elsevier
Publishing Place
New York
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Institute of Diabetes and Cancer (IDC)