J Korean Soc Hypertens.
2010 Mar;16(1):8-17.
The Effect of Bradykinin on High-Glucose Induced Apoptosis in Cultured Podocytes
- Affiliations
-
- 1BK21 Project for Medical Science, College of Medicine, Yonsei University, Seoul, Korea.
- 2Department of Internal Medicine, College of Medicine, Yonsei University, Seoul, Korea.
- 3Department of Internal Medicine, School of Medicine, Ewha Womans University, Seoul, Korea. drryu@ewha.ac.kr
Abstract
- BACKGROUND
In this study, we examined whether a local kallikrein-kinin system (KKS) exists in podocytes and whether expression of the components of the KKS and bradykinin (BK) production are changed in cultured podocytes exposed to high glucose medium. We also investigated the functional role of BK in podocyte apoptosis.
METHODS
Immortalized mouse podocytes were cultured in media containing normal glucose (5.6 mM, NG), NG+24.4 mM mannitol (NG+M), and high glucose (30 mM, HG) with or without pretreatment with 10(-8) M BK. BK levels were measured and mRNA and protein expression for all components of the KKS were evaluated. For assessment of apoptosis, western blots and Hoechst 33342 staining were done.
RESULTS
In cultured podocytes exposed to HG medium compared to NG cells, we found decreases not only in kininogen, kallikrein, BK B1-receptor (B1R), and B2-receptor (B2R) mRNA and protein expression, but also in BK levels. Changes in expression of apoptosis-related molecules and in the number of apoptotic cells in HG-stimulated podocytes were significantly abrogated by BK treatment. BK also inhibited activation of the proapoptotic p38 mitogen-activated protein kinase induced by HG.
CONCLUSION
The expression of all components of the KKS is decreased in cultured podocytes exposed to HG. In addition, BK treatment ameliorates podocyte apoptosis. These findings suggest that BK may be beneficial in preventing podocyte loss in diabetic nephropathy.
Keyword
- Full Text Links
-
- Actions
-
Cited
- CITED
-
- Close
- Share
-
- Similar articles
-
- Angiotensin II Receptor Blocker Induced Inhibition of Cellular Hypertrophy and Differential Expression of Cyclin-dependent Kinase Inhibitors in Cultured Podocytes Stimulated by Long-term High Glucose
- Mechanism of Podocyte Injury in Diabetic Nephropathy
- Interleukin-13 Increases Podocyte Apoptosis in Cultured Human Podocytes
- The Effect of High Glucose and TGF-beta on the Cellular Injury in Cultured Glomerular Epithelial Cells
- High glucose diets shorten lifespan of Caenorhabditis elegans via ectopic apoptosis induction
