Interferon-γ modulates the fibrinolytic response in cultured human endothelial cells

Arnman, Veronika; Stemme, Sten; Rymo, Lars; Risberg, Bo

doi:10.1016/0049-3848(95)93879-5

Cited by 29 publications

(15 citation statements)

References 16 publications

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“…Singh and colleagues (35) demonstrated that the absence of uPA impaired thrombus resolution, indicating the essential involvement of plasmin system in thrombus resolution. Evidence is accumulating to indicate that IFN-γ regulated the gene expression of plasminogen activators and their inhibitor (36)(37)(38)(39). However, in the present study, there was no significant difference in the intrathrombotic gene expression of uPA, tPA, and PAI-1 between WT and Ifng -/-mice.…”

Section: Ifn-γ/stat1 Signal Pathway Negatively Regulated the Gene Expcontrasting

confidence: 53%

Absence of IFN-γ accelerates thrombus resolution through enhanced MMP-9 and VEGF expression in mice

Nosaka¹,

Ishida²,

Kimura³

et al. 2011

J. Clin. Invest.

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Section: Ifn-γ/stat1 Signal Pathway Negatively Regulated the Gene Expcontrasting

confidence: 53%

Absence of IFN-γ accelerates thrombus resolution through enhanced MMP-9 and VEGF expression in mice

Nosaka¹,

Ishida²,

Kimura³

et al. 2011

J. Clin. Invest.

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“…Precursors of insulin at high concentrations in the plasma of patients with such conditions may directly stimulate PAI-1 synthesis [23]. Other stimu lants for PAI-1 induction in endothelial cells are TNF-a, lipopolysaccharide [24] and inter leukin-1 a [25], TNF-a induces PAI-1. ICAM-1 and VCAM-1 as a characteristic set of genes through activation of the transcription factor NF-k B [5].…”

Section: Pai-i Icam-1 and Vcam-1 In Werner Syndromementioning

confidence: 99%

Increased Blood Plasminogen Activator Inhibitor-1 and Intercellular Adhesion Molecule-1 as Possible Risk Factors of Atherosclerosis in Werner Syndrome

Murano

Nakazawa²,

Masuda³

et al. 1997

Gerontology

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Werner syndrome is a rare premature aging syndrome accompanied by severe atherosclerosis. The etiology of atherosclerosis is suspected to be due to its complications, namely diabetes mellitus, hyperinsulinemia and hyperlipidemia. But from an autopsy case we found that some other risk factors may be involved in the mechanism of atherosclerosis in this syndrome. Previously we revealed that the plasminogen activator inhibitor-1 (PAI-1) gene was being overexpressed in skin fibroblasts from a patient with this syndrome. PAI-1 is a potent inhibitor of tissue plasminogen activator and a possible risk factor of atherosclerosis. This led us to assess the plasma concentration of PAI-1. Our working hypothesis was that the PAI-1 gene was upregulated or not fully suppressed in cells responsible for the production of PAI-1 in plasma as well as in fibroblasts. The results show a high concentration of plasma PAI-1. One of the well-known physiological substances that induce the PAI-1 gene is tumor necrosis factor-α, which also induces other possible risk factors of atherosclerosis, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1. We found the serum concentrations of ICAM-1 to be elevated in patients with this syndrome. We conclude that high concentrations of PAI-1 and ICAM-1 in blood may be one of the potent causes of severe atherosclerosis in Werner syndrome.

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“…Furthermore, there are studies on the upregulation of PAI-1 in activated EC during the inflammatory response [67,73]. Like Arnman et al [71], Peiretti et al [74] observed an increase in PAI-1 expression in HUVEC after stimulation with LPS and TNF·, respectively. Mohamed et al [35] demonstrated that the expression of PAI mRNA in HUVEC is upregulated by TNF·.…”

mentioning

confidence: 99%

“…It is well known that thrombosis is a frequent complication of atherosclerosis and other conditions, in which inflammatory mediators are present in the vascular wall [71]. Shireman et al [72] found elevated levels of PAI-1 in atherosclerotic aorta and concluded that this might lead to an accumulation of extracellular matrix, thereby contributing to atherosclerosis.…”

mentioning

confidence: 99%

Comparative Analysis of the Reactivity of Human Umbilical Vein Endothelial Cells in Organ and Monolayer Culture

et al. 1999

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Endothelial monolayer cell cultures have been used to study pathomechanisms under standardized in vitro conditions. These results can only be regarded as valid as long as phenomena studied in vitro are comparable to findings in situ, e.g. in organ culture. The aim of the present study was to examine the reliability and comparability between human umbilical vein endothelial cells (HUVEC) in a monolayer cell culture model and endothelial cells (EC) in organ culture, as well as in the native umbilical cord. Our results prove the reliability of HUVEC as a model for standardized investigations of EC. The differences found suggest that gradual differences in antigen expression in vitro and in situ become apparent by comparing in situ and in vitro investigations.

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Interferon-γ modulates the fibrinolytic response in cultured human endothelial cells

Cited by 29 publications

References 16 publications

Absence of IFN-γ accelerates thrombus resolution through enhanced MMP-9 and VEGF expression in mice

Absence of IFN-γ accelerates thrombus resolution through enhanced MMP-9 and VEGF expression in mice

Increased Blood Plasminogen Activator Inhibitor-1 and Intercellular Adhesion Molecule-1 as Possible Risk Factors of Atherosclerosis in Werner Syndrome

Comparative Analysis of the Reactivity of Human Umbilical Vein Endothelial Cells in Organ and Monolayer Culture

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