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Targeting Dynamin 2 as a Novel Pathway to Inhibit Cardiomyocyte Apoptosis Following Oxidative Stress
Danchen Gao1, Jian Yang, Yutao Wu
1Department of Cardiology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Background/Aims:
Inhibition of Drp-1-mediated mitochondrial fission limits reactive oxygen species (ROS) production and apoptosis in cardiomyocytes subjected to ischemia/reperfusion injury. It remains unknown if Dynamin 2 inhibition results in similar protective effects. Here we studied the role of Dynamin 2 in cardiomyocyte oxidative stress-induced apoptosis and ROS production.
Methods:
The effect of lentiviral shRNA (lv5-shRNA) mediated Dynamin 2 knockdown on apopotosis, mitochondria, and ROS production were studied in neonatal mouse cardiomycytes, which were further treated with either selective Drp1 inhibitor mdivi-1 or the Dynamin 2/Drp1 inhibitor Dynasore. Apoptosis was evaluated by flow cytometry. Mitochondrial morphology and transmembrane potential (ΔΨm) were studied by confocal microscopy, and ROS production was detected by dichlorofluorescein diacetate.
Results:
Inhibition of Drp1 and Dynamin 2 protected against mitochondrial fragmentation, maintained ΔΨm, attenuated cellular ROS production and limited apoptosis. Moreover, Lv5-shRNA mediated knockdown of Dynamin 2 alleviated mitochondrial fragmentation, and reduced both ROS production and oxidative stress-induced apoptosis. The protective effects of Dynamin 2 knockdown were enhanced by Dynasore, indicating an added benefit.
Conclusions:
Oxidative stress-induced apoptosis and ROS production are attenuated by not only Drp1 inhibition but also Dynamin 2 inhibition, implicating Dynamin 2 as a mediator of oxidative stress in cardiomyocytes.
Insights
Dynamin 2 inhibition protects cardiomyocytes from oxidative stress by reducing reactive oxygen species (ROS) and apoptosis. This finding highlights Dynamin 2 as a key mediator in cardiomyocyte oxidative injury.
Area of Science:
- Cardiovascular Biology
- Mitochondrial Dynamics
- Cellular Stress Response
Background:
- Drp-1 inhibition mitigates ischemia/reperfusion injury in cardiomyocytes by limiting ROS and apoptosis.
- The role of Dynamin 2 in cardiomyocyte oxidative stress remains largely unexplored.
Purpose of the Study:
- To investigate the protective effects of Dynamin 2 inhibition against oxidative stress-induced apoptosis and ROS production in cardiomyocytes.
- To compare the effects of Dynamin 2 inhibition with Drp1 inhibition.
Main Methods:
- Neonatal mouse cardiomyocytes were subjected to oxidative stress.
- Dynamin 2 was inhibited using lentiviral shRNA (lv5-shRNA).
- Cells were treated with Drp1 inhibitor (mdivi-1) or Dynamin 2/Drp1 inhibitor (Dynasore). Apoptosis, mitochondrial morphology, transmembrane potential (ΔΨm), and ROS production were assessed.
Main Results:
- Inhibition of both Drp1 and Dynamin 2 attenuated mitochondrial fragmentation, preserved ΔΨm, reduced ROS, and decreased apoptosis.
- Dynamin 2 knockdown alone alleviated mitochondrial fragmentation and reduced ROS production and apoptosis.
- Combined inhibition with Dynasore enhanced the protective effects of Dynamin 2 knockdown.
Conclusions:
- Dynamin 2 inhibition, similar to Drp1 inhibition, attenuates oxidative stress-induced apoptosis and ROS production in cardiomyocytes.
- Dynamin 2 plays a significant role as a mediator of oxidative stress in the heart.
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