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Catalase overexpression attenuates angiotensinogen expression and apoptosis in diabetic mice
M-L Brezniceanu1, F Liu, C-C Wei
1Research Centre, Centre hospitalier de l'Université de Montréal (CHUM)-Hôtel-Dieu, Montreal, Quebec, Canada.
Abstract:
Increased generation of reactive oxygen species (ROS) leads to oxidative stress in diabetes. Catalase is a highly conserved heme-containing protein that reduces hydrogen peroxide to water and oxygen and is an important factor decreasing cellular injury owing to oxidative stress. Hyperglycemic conditions increase oxidative stress and angiotensinogen gene expression. Angiotensinogen conversion to angiotensin II leads to a furtherance in oxidative stress through increased generation of reactive oxygen species. In this study, we utilized mice transgenically overexpressing rat catalase in a kidney-specific manner to determine the impact on ROS, angiotensinogen and apoptotic gene expression in proximal tubule cells of diabetic animals. Proximal tubules isolated from wild-type and transgenic animals without or with streptozotocin-induced diabetes were incubated in low glucose media in the absence or presence of angiotensin II or in a high-glucose media. Our results show that the overexpression of catalase prevents the stimulation of ROS and angiotensinogen mRNA in tubules owing to elevated glucose or angiotensin II in vitro. Additionally, overexpression of catalase attenuated ROS generation, angiotensinogen and proapoptotic gene expression and apoptosis in the kidneys of diabetic mice in vivo. Our studies point to an important role of ROS in the pathophysiology of diabetic nephropathy.
Insights
Overexpressing catalase in kidneys reduces oxidative stress and harmful gene expression in diabetic mice. This highlights catalase
Area of Science:
- Biochemistry
- Molecular Biology
- Nephrology
Background:
- Diabetes mellitus is characterized by increased reactive oxygen species (ROS) production, leading to oxidative stress.
- Catalase, an enzyme that neutralizes hydrogen peroxide, plays a crucial role in mitigating cellular damage from oxidative stress.
- Hyperglycemia in diabetes exacerbates oxidative stress and upregulates angiotensinogen, further increasing ROS.
Purpose of the Study:
- To investigate the protective effects of kidney-specific catalase overexpression against oxidative stress and related gene expression in diabetic conditions.
- To determine the impact of catalase on ROS, angiotensinogen, and apoptotic pathways in proximal tubule cells of diabetic mice.
Main Methods:
- Utilized transgenic mice with kidney-specific overexpression of rat catalase.
- Induced diabetes using streptozotocin in both wild-type and transgenic mice.
- Incubated isolated proximal tubules in vitro under varying glucose and angiotensin II conditions.
- Assessed ROS generation, angiotensinogen mRNA, proapoptotic gene expression, and apoptosis in vivo and in vitro.
Main Results:
- Catalase overexpression prevented the increase in ROS and angiotensinogen mRNA induced by high glucose or angiotensin II in vitro.
- In diabetic mice, catalase overexpression significantly reduced ROS generation, angiotensinogen mRNA, and proapoptotic gene expression in the kidneys.
- Catalase overexpression also attenuated apoptosis in the kidneys of diabetic mice.
Conclusions:
- Kidney-specific catalase overexpression effectively mitigates oxidative stress and related cellular damage in diabetic nephropathy.
- Reactive oxygen species play a significant role in the development and progression of diabetic kidney disease.
- Targeting ROS through enzymes like catalase may offer a therapeutic strategy for diabetic nephropathy.
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