Key result
Inhibition of miR-199a-3p and -5p independently increases NO bioavailability by promoting eNOS activity and reducing its degradation, supporting VEGF-induced endothelial tubulogenesis.
Population
Bovine aortic endothelial cells and mice
Design
Preclinical
Follow-up
2 weeks (for angiotensin infusion)
Authors
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miR-199a regulates endothelial eNOS/NO; leaves open therapeutic targeting in vascular dysfunction.
Inhibition of miR-199a-3p and -5p enhances endothelial nitric oxide bioavailability and promotes angiogenesis, suggesting a potential therapeutic target for endothelial dysfunction.
Joris et al. (2018) studied Endothelial function. Inhibition of miR-199a-3p and -5p was evaluated on eNOS activity and NO bioavailability. Inhibition of miR-199a-3p and -5p independently increases NO bioavailability by promoting eNOS activity and reducing its degradation, supporting VEGF-induced endothelial tubulogenesis.
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