This study investigates the effects of overexpressing human NADPH oxidase 5 (NOX5) in aortic endothelial cells, focusing on its role in inducing cyclooxygenase-2 (COX-2) expression and the subsequent production of prostaglandin E2 (PGE2). The research aims to elucidate the molecular mechanisms by which NOX5-derived reactive oxygen species (ROS) influence inflammatory pathways in vascular endothelial cells.
Overexpression of NOX5 in aortic endothelial cells led to increased COX-2 expression and elevated levels of PGE2, mediated through the activation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway. These findings suggest that NOX5-derived ROS play a significant role in modulating inflammatory responses in endothelial cells, which may contribute to cardiovascular pathologies.
The study utilized a conditional endothelial-specific NOX5 Knockin mouse model developed in collaboration with genOway. This model allows for the controlled overexpression of human NOX5 specifically in endothelial cells, enabling the assessment of its impact on vascular function and inflammatory responses.
Cardiovascular diseases, Endothelial inflammation, Oxidative stress, Prostaglandin synthesis, Vascular biology
Conditional Knockin, Endothelial-specific expression, Inducible gene overexpression, ROS measurement, Inflammatory pathway analysis
From model design to experimental results
Tailor-made solutions adapted to scientific questions
Comprehensive dataset package
Generated with biopharma partners and in-house
Scientific follow-up and advice along the project
Collaborative approach for problem solving and development of innovative models
Breeding facilities in US and Europe
Certified health status from professional breeders
