ACE2 and Oxidative Stress in the Brain
Author Information
Author(s): Xia Huijing, Suda Sonia, Bindom Sharell, Feng Yumei, Gurley Susan B., Seth Dale, Navar L. Gabriel, Lazartigues Eric
Primary Institution: Louisiana State University Health Sciences Center
Hypothesis
By transforming Angiotensin-II (AngII) into Ang-(1–7), ACE2 might reduce AngII-mediated oxidative stress in the brain and prevent autonomic dysfunction.
Conclusion
ACE2 gene deletion promotes age-dependent oxidative stress, autonomic dysfunction, and hypertension, while ACE2 gene therapy decreases ROS formation and improves autonomic function.
Supporting Evidence
- ACE2 overexpression resulted in a reduction of reactive oxygen species (ROS) formation.
- ACE2 gene therapy to the PVN reduced AngII-mediated increase in NADPH oxidase activity.
- ACE2 deletion led to increased sympathetic tone and autonomic dysfunction.
- ACE2 gene therapy improved autonomic function in ACE2−/y mice.
Takeaway
ACE2 helps keep our heart and blood pressure healthy by reducing harmful substances in the brain. When ACE2 is missing, it can lead to more stress and problems with how our body controls blood pressure.
Methodology
The study involved in vitro experiments with Neuro2A cells and in vivo experiments with ACE2 knockout mice to assess the effects of ACE2 on oxidative stress and autonomic function.
Limitations
The study did not show an increase in plasma and brain AngII levels despite a lack of ACE2, which may be due to the sensitivity of the measurement approach.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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