Journal
SCIENCE
Volume 308, Issue 5728, Pages 1618-1621Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1108228
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Funding
- NHLBI NIH HHS [K08 HL004171-05, HL004171, K08 HL004171] Funding Source: Medline
- NIEHS NIH HHS [P01 ES012496-010004, ES012496, P01 ES012496] Funding Source: Medline
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Mechanisms that protect against asthma remain poorly understood. S-nitrosoglutathione (GSNO), an endogenous bronchodilator, is depleted from asthmatic airways, suggesting a protective role. We report that, following allergen challenge, witd-type mice exhibiting airway hyperresponsivity have increased airway levels of the enzyme GSNO reductase (GSNOR) and are depleted of lung S-nitrosothiols (SNOs). In contrast, mice with genetic deletion of GSNOR exhibit increases in lung SNOs and are protected from airway hyperresponsivity. Our results indicate that endogenous SNOs, governed by GSNOR, are critical regulators of airway responsivity and may provide new therapeutic approaches to asthma.
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