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Antioxidants ameliorate the expression of vascular endothelial growth factor mediated by protein kinase C in diabetic
Eun-Young Lee1, Choon Hee Chung, Jung Hyun Kim
1Department of Internal Medicine and Clinical Research Institute, Soon Chun Hyang University Cheonan Hospital, Cheonan, Korea.
Background:
The increased production of reactive oxygen species (ROS) may be involved in the onset or development of diabetic vascular complications. The release of ROS from podocytes plays a role in the pathogenesis of glomerular damage in various experimental glomerular diseases. Although it is assumed that the podocyte injury also plays an important role in diabetic nephropathy, the mechanism is still unknown.
Methods:
Using a differentiated mouse podocyte cell line, we investigated: (1) whether a high level of ambient glucose increases the level of ROS, (2) whether the protein kinase C (PKC) pathway is involved in a high-glucose-induced generation of ROS and vascular endothelial growth factor (VEGF) and (3) whether antioxidants ameliorate PKC-mediated VEGF expression in diabetic milieu.
Results:
Intracellular ROS generation was significantly higher in high glucose than in control conditions in cultured podocytes. High ambient glucose also increased VEGF mRNA and protein expression. The high-glucose-induced increases in ROS and VEGF mRNA and protein by podocytes were effectively inhibited by pretreatment with various antioxidants and were completely restored by PKC inhibition. The results show that cultured mouse podocytes produce ROS in response to high glucose, and that PKC is involved in high-glucose-induced ROS and VEGF production by podocyte.
Conclusion:
Increased ROS in podocytes may play a role in the pathogenesis of podocyte injury in diabetic nephropathy.
Insights
High glucose levels increase reactive oxygen species (ROS) and vascular endothelial growth factor (VEGF) in kidney podocytes, a process mediated by protein kinase C (PKC). Antioxidants can mitigate these effects, suggesting a role for ROS in diabetic nephropathy.
Area of Science:
- Nephrology
- Diabetology
- Cell Biology
Background:
- Diabetic nephropathy is a major complication of diabetes, characterized by glomerular damage.
- Increased reactive oxygen species (ROS) production is implicated in diabetic vascular complications.
- Podocyte injury is believed to contribute to diabetic nephropathy, but the underlying mechanisms are unclear.
Purpose of the Study:
- To investigate if high ambient glucose increases ROS levels in podocytes.
- To determine the involvement of the protein kinase C (PKC) pathway in high-glucose-induced ROS and vascular endothelial growth factor (VEGF) generation.
- To examine if antioxidants can ameliorate PKC-mediated VEGF expression in a diabetic context.
Main Methods:
- Utilized a differentiated mouse podocyte cell line.
- Exposed cells to high glucose conditions and measured intracellular ROS generation.
- Assessed VEGF mRNA and protein expression.
- Investigated the effects of antioxidants and PKC inhibitors.
Main Results:
- High glucose significantly increased intracellular ROS generation in cultured podocytes.
- Elevated glucose also enhanced VEGF mRNA and protein expression.
- Antioxidants and PKC inhibition effectively reduced high-glucose-induced ROS and VEGF production.
Conclusions:
- Cultured mouse podocytes produce ROS in response to high glucose.
- The protein kinase C (PKC) pathway is involved in high-glucose-induced ROS and VEGF production.
- Increased ROS in podocytes may contribute to the pathogenesis of podocyte injury in diabetic nephropathy.
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