The kidney is a major site of alpha(2)-antiplasmin production.

Menoud, Pierre-Alain; Sappino, N; Boudal-Khoshbeen, M; Vassalli, J.-D.; Sappino, André‐Pascal

doi:10.1172/jci118694

Cited by 61 publications

(53 citation statements)

References 41 publications

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“…Lungs from saline-washed mice were dissected, frozen immediately in liquid nitrogen, and stored at Ϫ 80 Њ C. After homogenization in guanidinium/thiocyanate, total RNA was isolated by cesium chloride centrifugation as described previously (13). uPA, tPA, PAI-1, PAI-2, ␣ 2-antiplasmin ( ␣ 2-AP), and protease-nexin I (PN-I) probes were prepared as described (14)(15)(16)(17)(18) and transcribed in vitro using ␣ 32 P-labeled UTP (specific activity 400 Ci/mmol; Amersham International, Buckinghamshire, United Kingdom). RNase protection assays were performed as described (19).…”

Section: Methodsmentioning

confidence: 99%

Plasminogen activator inhibitor-1 in acute hyperoxic mouse lung injury.

Barazzone-Argiroffo

Belin²,

Piguet³

et al. 1996

J. Clin. Invest.

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127

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Hyperoxia-induced lung disease is associated with prominent intraalveolar fibrin deposition. Fibrin turnover is tightly regulated by the concerted action of proteases and antiproteases, and inhibition of plasmin-mediated proteolysis could account for fibrin accumulation in lung alveoli. We show here that lungs of mice exposed to hyperoxia overproduce plasminogen activator inhibitor-1 (PAI-1), and that PAI-1 upregulation impairs fibrinolytic activity in the alveolar compartment. To explore whether increased PAI-1 production is a causal or only a correlative event for impaired intraalveolar fibrinolysis and the development of hyaline membrane disease, we studied mice genetically deficient in PAI-1. We found that these mice fail to develop intraalveolar fibrin deposits in response to hyperoxia and that they are more resistant to the lethal effects of hyperoxic stress. These observations provide clear and novel evidence for the pathogenic contribution of PAI-1 in the development of hyaline membrane disease. They identify PAI-1 as a major deleterious mediator of hyperoxic lung injury. ( J. Clin. Invest. 1996. 98:2666-2673.)

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Section: Methodsmentioning

confidence: 99%

Plasminogen activator inhibitor-1 in acute hyperoxic mouse lung injury.

Barazzone-Argiroffo

Belin²,

Piguet³

et al. 1996

J. Clin. Invest.

Self Cite

127

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“…Other regulators, such as ␣-2 anti-plasmin, might be more critical (60,98). Plasmin has several proteolytic targets and can trigger receptor-dependent effects, and, together, its activities favor fibrosis development, at least in the UUO model.…”

Section: Plasminmentioning

confidence: 99%

Plasminogen Activator Inhibitor-1 in Chronic Kidney Disease

Eddy

Fogo

2006

Journal of the American Society of Nephrology

212

189

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“…Under normal conditions, the only fibrinolytic inhibitor that is detected in significant quantities in the kidney is ␣ 2 -antiplasmin (111), although low levels of protease nexin-1 and protein C inhibitor have been reported in mouse mesangial cells and human tubular cells, respectively (116,140). Not normally expressed in the kidney, PAI-1 is rapidly induced in a variety of acute and chronic renal diseases.…”

mentioning

confidence: 99%

Plasminogen activator inhibitor-1 and the kidney

Eddy

2002

American Journal of Physiology-Renal Physiology

174

132

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Plasminogen activator inhibitor-1 (PAI-1) is a serine protease inhibitor that was isolated 20 years ago. First recognized as an inhibitor of intravascular fibrinolysis, it is now evident that PAI-1 is a multifunctional protein with actions that may be dependent on or independent of its protease inhibitory effects. The latter often involve interactions between PAI-1 and vitronectin or the urokinase receptor. The protease-inhibitory actions of PAI-1 extend beyond fibrinolysis and include extracellular matrix turnover and activation of several proenzymes and latent growth factors. PAI-1 has been implicated in several renal pathogenetic processes, including thrombotic microangiopathies and proliferative and/or crescentic glomerulopathies. Most recently, it has become clear that PAI-1 also plays a pivotal role in progressive renal disease, both glomerulosclerosis and tubulointerstitial fibrosis. An active area of present research interest, untold stories are likely to be uncovered soon.

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The kidney is a major site of alpha(2)-antiplasmin production.

Cited by 61 publications

References 41 publications

Plasminogen activator inhibitor-1 in acute hyperoxic mouse lung injury.

Plasminogen activator inhibitor-1 in acute hyperoxic mouse lung injury.

Plasminogen Activator Inhibitor-1 in Chronic Kidney Disease

Plasminogen activator inhibitor-1 and the kidney

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