Key result
Gene transfer of eNOS to vascular rings of eNOS-deficient mice restored relaxation to acetylcholine and calcium ionophore, improving vascular function.
Why the study?
Does gene transfer of eNOS restore vascular relaxation in aortic rings from eNOS-deficient mice?
Population
Aortic rings from endothelial nitric oxide synthase (eNOS)-deficient (eNOS -/-) and wild-type (eNOS +/+) mice
Comparison
In vitro exposure to adenoviral vectors encoding… vs Vehicle or adenoviral vectors encoding…
Design
Preclinical
Authors
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eNOS gene transfer rescues vascular relaxation in deficient mouse models; leaves open translation to human endothelial dysfunction.
Does gene transfer of eNOS restore vascular relaxation in aortic rings from eNOS-deficient mice?
Gene transfer of eNOS can restore endothelium-dependent vascular relaxation in eNOS-deficient mice, demonstrating that vascular function can be improved by gene transfer when a major relaxation mechanism is genetically absent.
Lake-Bruse et al. (1999) studied eNOS deficiency. Gene transfer of eNOS (adenoviral vectors encoding eNOS) vs. Vehicle or adenoviral vectors encoding beta-galactosidase (lacZ) was evaluated on Relaxation to acetylcholine (ACh) and calcium ionophore (A-23187). Gene transfer of eNOS to vascular rings of eNOS-deficient mice restored relaxation to acetylcholine and calcium ionophore, improving vascular function.
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