Key result
Human PRR over-expression significantly increased ROS levels and NADPH oxidase activity in neuronal cells through both angiotensin II-dependent and -independent mechanisms.
p-value: p=<0.05
Human PRR over-expression induces ROS production in neuronal cells through both Ang II-dependent and -independent mechanisms, providing a potential new pathway for oxidative stress in the central nervous system.
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Hypothesis-generating for PRR as a neuronal oxidative stress target; should not yet change clinical practice.
Peng et al. (2013) studied Oxidative stress in neuronal cells. Adeno-associated virus encoding human PRR (AAV-hPRR-eGFP) vs. Control virus (AAV-eGFP) was evaluated on Reactive oxygen species (ROS) levels and NADPH oxidase activity (p=<0.05). Human PRR over-expression significantly increased ROS levels and NADPH oxidase activity in neuronal cells through both angiotensin II-dependent and -independent mechanisms.
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