Key result
Antisense oligonucleotide knockdown of arginase I in aortic rings from old rats significantly decreased arginase activity and enhanced calcium-dependent NOS activity and vasorelaxation.
Why the study?
Does knockdown of Arginase I using antisense oligonucleotides improve NO signaling and vasoreactivity in aortic rings from old rats?
Population
Aortic rings from 22-month-old rats
Comparison
Antisense oligonucleotide to knockdown arginase… vs Sense (S) oligonucleotides or medium alone (C)
Design
Preclinical
Follow-up
24 hours
Authors
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Enhances endothelial function in aged rat aortas; leaves open therapeutic translation of arginase I inhibition to human vascular aging.
Does knockdown of Arginase I using antisense oligonucleotides improve NO signaling and vasoreactivity in aortic rings from old rats?
Knockdown of Arginase I using antisense oligonucleotides restores NO signaling and improves endothelial function in aged rat vasculature, suggesting a potential therapeutic target for age-related vascular dysfunction.
White et al. (2005) studied Age-related endothelial dysfunction. Antisense (AS) oligonucleotide against arginase I vs. Sense (S) oligonucleotides or medium alone (C) was evaluated on Arg I protein knockdown, arginase activity, NOS activity, and vasorelaxant responses. Antisense oligonucleotide knockdown of arginase I in aortic rings from old rats significantly decreased arginase activity and enhanced calcium-dependent NOS activity and vasorelaxation.
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