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Titolo:
Paradoxical rescue from ischemic lung injury by inhaled carbon monoxide driven by derepression of fibrinolysis
Autore:
Fujita, T; Toda, K; Karimova, A; Yan, SF; Naka, Y; Yet, SF; Pinsky, DJ;
Indirizzi:
Columbia Univ, Coll Phys & Surg, New York, NY 10032 USA Columbia Univ NewYork NY USA 10032 l Phys & Surg, New York, NY 10032 USA Brigham & Womens Hosp, Div Cardiovasc, Boston, MA 02115 USA Brigham & Womens Hosp Boston MA USA 02115 ardiovasc, Boston, MA 02115 USA
Titolo Testata:
NATURE MEDICINE
fascicolo: 5, volume: 7, anno: 2001,
pagine: 598 - 604
SICI:
1078-8956(200105)7:5<598:PRFILI>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN SKIN FIBROBLASTS; SMOOTH-MUSCLE CELLS; HEME OXYGENASE-1; NITRIC-OXIDE; OXIDATIVE STRESS; ISCHEMIA/REPERFUSION INJURY; PROVIDES PROTECTION; UP-REGULATION; NULL MICE; GENE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Pinsky, DJ Columbia Univ, Coll Phys & Surg, New York, NY 10032 USA Columbia Univ New York NY USA 10032 rg, New York, NY 10032 USA
Citazione:
T. Fujita et al., "Paradoxical rescue from ischemic lung injury by inhaled carbon monoxide driven by derepression of fibrinolysis", NAT MED, 7(5), 2001, pp. 598-604

Abstract

Carbon monoxide (CO) can arrest cellular respiration, but paradoxically, it is synthesized endogenously by heme oxygenase type 1 (Ho-1) in response to ischemic stress. Ho-1-deficient (Hmox1(-/-)) mice exhibited lethal ischemic lung injury, but were rescued from death by inhaled CO. CO drove ischemic protection by activating soluble guanylate cyclase and thereby suppressedhypoxic induction of the gene encoding plasminogen activator inhibitor-1 (PAI-1) in mononuclear phagocytes, which reduced accrual of microvascular fibrin. GO-mediated ischemic protection observed in wild-type mice was lost in mice null for the gene encoding PAI-1 (Serpine1). These data establish a fundamental link between CO and prevention of ischemic injury based on the ability of CO to derepress the fibrinolytic axis. These data also point to a potential therapeutic use for inhaled CO.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/04/20 alle ore 11:48:40