Identification of the inhibitor of the plasminogen activator as the major protein secreted by endothelial rat liver cells

Kuiper, Johan; Kamps, Jan A. A. M.; Berkel, Theo J.C. Van

doi:10.1016/0014-5793(89)80227-3

Cited by 14 publications

(4 citation statements)

References 20 publications

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“…Therefore, it would seem likely that these cells synthesize PAI-l in vivo. These results have confirmed previous studies performed in the rat showing the contribution of endothelial liver cells to the production of PAI-l, (32,33). The absence of labeling in the experimental controls shows that the signal observed corresponds to pure specific P AI -I messengers.…”

Section: Pai-l Localization In the Liversupporting

confidence: 91%

Plasminogen Activator Inhibitor-1 Expression in Human Liver and Healthy or Atherosclerotic Vessel Walls

et al. 1994

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SummaryIndividuals with elevated levels of plasminogen activator inhibitor type 1 are at risk of developing atherosclerosis. The mechanisms leading to increased plasma PAI-1 concentrations are not well understood. The link observed between increased PAI-1 levels and insulin resistance has lead workers to investigate the effects of insulin or triglyceride rich lipoproteins on PAI-1 production by cultured hepatocytes or endothelial cells. However, little is known about the contribution of these cells to PAI-1 production in vivo. We have studied the expression of PAI-1 in human liver sections as well as in vessel walls from different territories, by immunocytochemistry and in situ hybridization.We have observed that normal liver endothelial cells expressed PAI-1 while parenchymal cells did not. However, this fact does not refute the role of parenchymal liver cells in pathological states.In healthy vessels, PAI-1 mRNA and protein were detected primarily at the endothelium from the lumen as well as from the vasa vasorum. In normal arteries, smooth muscle cells were able to produce PAI-1 depending on the territory tested. In deeply altered vessels, PAI-1 expression was observed in neovessels scattering the lesions, in some intimal cells and in smooth muscle cells. Local increase PAI-1 mRNA described in atherosclerotic lesions could be due to the abundant neovascularization present in the lesion as well as a raised expression in smooth muscle cells. The increased PAI-1 in atherosclerosis could lead to fibrin deposit during plaque rupture contributing further to the development and progression of the lesion.

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Section: Pai-l Localization In the Liversupporting

confidence: 91%

Plasminogen Activator Inhibitor-1 Expression in Human Liver and Healthy or Atherosclerotic Vessel Walls

et al. 1994

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“…There fore, the decreased PAA in the liver should be, at least partly, due to the increased PI which the lead compounds have induced. Interestingly, the PAI in the liver has not been affected, although this organ is a site of PA inhibitor production [44], The in vivo dissociation of the responses of PI and PAI in the same organ to the effect of an exoge nous factor has also been seen in other cases [32]. In the developing brain PAA is in volved in at least two steps of neuro-onto genesis, neuronal migration and astrocytic proliferation [45].…”

Section: Discussionmentioning

confidence: 99%

Transplacental Effect of Lead Compounds on Tissue Plasminogen Activator Activity, Plasminogen Activator Inhibition and Plasmin Inhibition

Smokovitis

Kokolis²,

Alexaki³

et al. 1990

Neonatology

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The transplacental effect of lead compounds (lead acetate and tetraethyl lead) on the tissue plasminogen activator activity (PAA), plasminogen activator inhibition (PAI) and plasmin inhibition (PI) was studied in the rat. The concentration of lead in organs of the newborn showed a great variation; the distribution of lead in the organs studied depended on the dose and the stage of gestation at injection. In each organ the concentration of lead was dose-dependent. In control specimens no lead could be detected. The tissue response of PAA, PAI and PI to the lead compounds also showed a great variation; however, there was no correlation between lead concentrations and PAA, PAI or PI responses. Changes of one or more of the parameters studied (PAA, PAI or PI) were noticed in lungs, liver, heart, brain and kidneys. The PAA was due to the tissue type plasminogen activator in all organs studied; in kidneys and lungs the urokinase type of plasminogen activator was also detected. Therefore, fetal tissue PAA, PAI and PI can be affected transplacentally by lead compounds.

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“…Células endoteliais e HSCs, têm sido identificadas como as maiores liberadoras da PAI I (KUIPER et al, 1989;ZHANG et al, 1999) , apesar dos hepatócitos apresentarem alguma expressão quando submetidos a alguma toxina (QUAX et al, 1990). HSC também produzem uPA e uPAR em culturas primárias (LEYLAND et al, 1996).…”

Section: Mmp 1 8 E 13 (Colagenases)unclassified

Efeito do tratamento com fatores hepatotróficos em ratas (Wistar) induzidas experimentalmente à cirrose por Tioacetamida

Guerra¹

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Identification of the inhibitor of the plasminogen activator as the major protein secreted by endothelial rat liver cells

Cited by 14 publications

References 20 publications

Plasminogen Activator Inhibitor-1 Expression in Human Liver and Healthy or Atherosclerotic Vessel Walls

Plasminogen Activator Inhibitor-1 Expression in Human Liver and Healthy or Atherosclerotic Vessel Walls

Transplacental Effect of Lead Compounds on Tissue Plasminogen Activator Activity, Plasminogen Activator Inhibition and Plasmin Inhibition

Efeito do tratamento com fatores hepatotróficos em ratas (Wistar) induzidas experimentalmente à cirrose por Tioacetamida

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