Cell specific control of coagulation and fibrinolysis within the lung

Sisson, Thomas H.; Simon, Richard H.

doi:10.1160/th04-06-0354

Thromb Haemost

2004

DOI: 10.1160/th04-06-0354

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Cell specific control of coagulation and fibrinolysis within the lung

Thomas H. Sisson¹,

Richard H. Simon²

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Cited by 3 publications

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“…2). The fibrinolytic activity that is normally present in bronchoalveolar lavage (BAL) fluid is depressed in patients with many types of lung injury due to increased levels of plasminogen activator inhibitors, particularly plasminogen activator inhibitor (PAI)-1 (3-7).…”

mentioning

confidence: 99%

Plasminogen-Mediated Activation and Release of Hepatocyte Growth Factor from Extracellular Matrix

Matsuoka

Sisson

Nishiuma

et al. 2006

Am J Respir Cell Mol Biol

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Interventions that enhance plasminogen activation within the lung consistently limit the fibrosis that follows alveolar injury. However, this protective effect cannot be attributed solely to accelerated clearance of fibrin that forms as a provisional matrix after lung injury. To explore other mechanisms, we considered interactions between the plasminogen activation system and hepatocyte growth factor (HGF). HGF is known to have antifibrotic activity, but to do so, it must be both released from its sites of sequestration within extracellular matrix (ECM) and activated by proteolytic cleavage. A recent study using bleomycin-exposed mice showed that manipulations of the plasminogen activation system influenced the amount of free HGF within bronchoalveolar lavage fluid without affecting total lung HGF mRNA or protein. To elucidate the mechanisms, we studied the role of plasminogen activation in fibroblastmediated HGF release and activation. We found that NIH3T3 and mouse lung fibroblasts release ECM-bound HGF in a plasminogendependent fashion. The plasminogen effect was lost when lung fibroblasts from urokinase-type plasminogen activator (uPA)-deficient mice were used, and was increased by fibroblasts from plasminogen activator inhibitor (PAI)-1-deficient mice. Plasminogen addition to NIH3T3 or mouse lung fibroblasts increased conversion of pro-HGF to its active form. The plasminogen effect on activation was lost when uPA-deficient fibroblasts were used and accentuated by PAI-1-deficient fibroblasts. In conjunction with the previous in vivo study, these results suggest that plasminogen activation can protect the lung against fibrosis by increasing the availability of active HGF.

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confidence: 99%

Plasminogen-Mediated Activation and Release of Hepatocyte Growth Factor from Extracellular Matrix

Matsuoka

Sisson

Nishiuma

et al. 2006

Am J Respir Cell Mol Biol

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Expression Profiling and Disseminated Intravascular Coagulation

Idell¹

2007

Am J Respir Crit Care Med

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The role of urokinase in idiopathic pulmonary fibrosis and implication for therapy

Gharaee−Kermani

Phan

et al. 2008

Expert Opinion on Investigational Drugs

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Cell specific control of coagulation and fibrinolysis within the lung

Cited by 3 publications

References 31 publications

Plasminogen-Mediated Activation and Release of Hepatocyte Growth Factor from Extracellular Matrix

Plasminogen-Mediated Activation and Release of Hepatocyte Growth Factor from Extracellular Matrix

Expression Profiling and Disseminated Intravascular Coagulation

The role of urokinase in idiopathic pulmonary fibrosis and implication for therapy

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