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Protection from experimental asthma by an endogenous bronchodilator.

Authors: Que, LG  Liu, L  Yan, Y  Whitehead, GS  Gavett, SH  Schwartz, DA  Stamler, JS 
Citation: Que LG, etal., Science. 2005 Jun 10;308(5728):1618-21. Epub 2005 May 26.
Pubmed: (View Article at PubMed) PMID:15919956
DOI: Full-text: DOI:10.1126/science.1108228

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, wild-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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CRRD Object Information
CRRD ID: 5128892
Created: 2011-03-22
Species: All species
Last Modified: 2011-03-22
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.