HqMOLYTIC-URqMIC SYNDROME: DEFICIENCY OF PLASMA FACTOR(S) REGULATING PROSTACYCLIN ACTIVITY?

Remuzzi, Giuseppe; Marchesi, D.; Mecca, G; Misiani, Rocco; Livio, M.; Gaetano, Giovanni de; Donati, Maria Benedetta

doi:10.1016/s0140-6736(78)91573-8

Cited by 283 publications

(52 citation statements)

References 9 publications

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“…17 -19 Patients with hemolytic uremic syndrome and related disorders, such as thrombotic thrombocytopenic purpura, lack of plasma factor that stimulates PGI 2 synthesis. 20 Plasma from a patient with "lupus anticoagulant" inhibited PGI 2 formation by vascular tissue. 21 Reductions or increases in PGI 2 production have been reported in patients with metabolic diseases such as diabetes and hyperlipidemia and in patients with documented atherosclerotic disease.…”

Section: Discussionmentioning

confidence: 99%

Prostacyclin production by endothelial cells. Effects of sera from normal and hyperlipidemic subjects.

et al. 1985

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The influence of hyperlipidemic sera on prostacyclin (PGI 2 ) production by cultured endothelial cells was assessed by comparing sera from three types of hyperlipidemias with sera from normal subjects. Sera prepared from normal whole blood (WBS), platelet-rich plasma (PRPS), and platelet-poor plasma (PPPS) were also compared. Bovine aortic endothelial cells (BAEC) incubated with 25% WBS increased PGI 2 synthesis significantly within 1 hour, with little further increase by 16 hours; human umbilical vein endothelial cells (HUEC) incubated with 25% WBS for 1 hour showed no elevation in PGI 2 , whereas PGI 2 levels increased substantially after 16 hours. PPPS and PRPS stimulated PGI 2 synthesis by BAEC equally at 1 hour. However, there was no rise in PGI 2 after PPPS in HUEC; PGI 2 rose after 16 hours with PRPS and rose further with WBS after 16 hours.Since WBS best enhanced PGI 2 production in human endothelial cells, it was chosen for comparison of the effects of hyperlipidemic and normolipidemic sera. PGI 2 synthesis by HUEC significantly increased upon incubation with WBS from Types Mb and IV patients in comparison to WBS from Type lla hypercholesterolemic patients or normal controls. In contrast, WBS from all these hyperlipidemic subjects stimulated PGI 2 synthesis by BAEC similarly to WBS from controls. We conclude that incubation of human endothelial cells with WBS containing high levels of atherogenic lipoproteins does not reduce PGI 2 formation by the cells. Moreover, the time course and the contribution of lipid, plasma, or cellular factors to PGI 2 formation vary according to the cell type tested. Caution should be exercised in extrapolating results achieved with serum and cells from the same species to other settings. shown that high density lipoproteins (HDL) can provide arachidonic acid for PGI 2 synthesis by porcine and human endothelial cells, while low density lipoproteins (LDL) apparently have a negligible effect under the same experimental conditions. 45 In other studies, incubation of human umbilical cord endothelial cells (HUEC) with low density lipoproteins diminished PGI 2 production, 6 but this effect may have reflected oxidation of LDL during isolation.7 Since endothelial cells in vivo are not exposed to isolated lipoprotein fractions, and little information is available on the effect of hyperlipidemic sera on PGI 2 production by endothelial cells, the influence of different serum lipoprotein patterns on PGI 2 formation by cells requires further examination. Clarification of such effects takes on clinical relevance in view of recent evidence that vascular PGI 2 may have an antiatherogenic effect both through regulation of cholesteryl ester deposition in vascular smooth muscle and through regulation of smooth muscle cell proliferation.

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Section: Discussionmentioning

confidence: 99%

Prostacyclin production by endothelial cells. Effects of sera from normal and hyperlipidemic subjects.

et al. 1985

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“…Prostacyclin, a potent vasodilator and inhibitor of platelet aggregation, has been found to be deficient in certain cases of HUS (174,175). Deficiency may be caused by low production secondary to damaged endothelium, or by high consumption, and may promote platelet aggregation.…”

Section: Prothrombotic Statementioning

confidence: 99%

Pathogenesis of Shiga Toxin-Associated Hemolytic Uremic Syndrome

2001

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“…60 - 62 This deficiency is postulated to be secondary to a lack of a 'plasma factor' which normally stimulates prostacyclin production. 5 A patient with TTP had an undetectable level of 6-oxo-PGF la (< 60 pg/ml) whereas the mean value in control subjects was 154 ± 48 pg/ml.…”

Section: Prostacyclin and Txa 2 In Diseasementioning

confidence: 99%