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Titolo:
Pulmonary fibrosis is increased in mice carrying the factor V Leiden mutation following bleomycin injury
Autore:
Xu, ZJ; Westrick, RJ; Shen, YC; Eitzman, DT;
Indirizzi:
Univ Michigan, Med Ctr, Dept Internal Med, Div Cardiol, Ann Arbor, MI 49109 USA Univ Michigan Ann Arbor MI USA 49109 Div Cardiol, Ann Arbor, MI 49109 USA
Titolo Testata:
THROMBOSIS AND HAEMOSTASIS
fascicolo: 3, volume: 85, anno: 2001,
pagine: 441 - 444
SICI:
0340-6245(200103)85:3<441:PFIIIM>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACTIVATED PROTEIN-C; RESPIRATORY-DISTRESS SYNDROME; ALVEOLAR FIBRIN DEPOSITION; INDUCED LUNG INJURY; VENOUS THROMBOSIS; LOCAL ABNORMALITIES; COAGULATION; RESISTANCE; GENE; PROCOAGULANT;
Keywords:
pulmonary fibrosis; thrombosis; bleomycin; factor V Leiden; fibrin;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
22
Recensione:
Indirizzi per estratti:
Indirizzo: Eitzman, DT Univ Michigan, Med Ctr, Dept Internal Med, Div Cardiol, 7301 MSRB 3,1150 WMed Ctr Dr, Ann Arbor, MI 49109 USA Univ Michigan 7301 MSRB 3,1150 W Med Ctr Dr Ann Arbor MI USA 49109
Citazione:
Z.J. Xu et al., "Pulmonary fibrosis is increased in mice carrying the factor V Leiden mutation following bleomycin injury", THROMB HAEM, 85(3), 2001, pp. 441-444

Abstract

Increased fibrin deposition following inflammatory lung injury has been proposed to facilitate,the development of pulmonary fibrosis. Therefore, factors predisposing to thrombosis may affect the fibrotic response to injury. Activated protein C (aPC) resistance due to the factor V Leiden mutation (FVL) is a common genetic risk factor for vascular thrombosis. To examine therelationship between aPC resistance and the development of pulmonary fibrosis, lung inflammation was induced by bleomycin in mice carrying the FVL mutation. Three weeks following the instillation of;0.0375 U of breomycin, the lungs of mice homozygous and heterozygous for FVL contained significantlymore hydroxyproline (35 +/- 4 and 36 +/- 7 ug hydroxyproline/ mg total protein, respectively) than wild-type mice (26 +/- 6 ug/mg protein, p <0.01 for both comparisons). These data demonstrate a strong relationship between aPC resistance and the pulmonary fibrosis that occurs following inflammatorylung injury.

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Documento generato il 10/07/20 alle ore 09:23:34