Intracellular processing of endothelial nitric oxide synthase isoforms associated with differences in severity of cardiopulmonary diseases: Cleavage of proteins with aspartate vs. glutamate at position 298
Population
Transfected cells (COS7), primary human endothelial cells, and human hearts
Comparison
eNOS with aspartate at position 298 (T genotype) vs eNOS with glutamate at position 298 (G genotype)
Design
Preclinical
Authors
Discussion
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Member takes
Implication
Supports functional relevance of eNOS Asp298 polymorphism in models; leaves open causal contribution to human cardiopulmonary disease.
Structured PICO
P
Population
Transfected cells (COS7), primary human endothelial cells, and human hearts
I
Intervention
eNOS with aspartate at position 298 (T genotype)
C
Comparator
eNOS with glutamate at position 298 (G genotype)
O
Outcome
Cleavage of eNOS protein into 100-kDa and 35-kDa productssurrogate
The eNOS 894 G/T polymorphism (Asp298) results in a protein susceptible to cleavage, demonstrating a direct functional effect of this polymorphism associated with cardiopulmonary disease severity.
Cite This Study
Tesauro et al. (2000) studied this question.