Endothelium-derived prostacyclin: effect of serum from women with normal and hypertensive pregnancy

1992 ◽  
Vol 82 (4) ◽  
pp. 383-388 ◽  
Author(s):  
Vivienne C. Zammit ◽  
Judith A. Whitworth ◽  
Mark A. Brown
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Pregnant Women ◽  
Cell Injury ◽  
Umbilical Vein ◽  
Pregnancy Induced Hypertension ◽  
Intact Cells ◽  
Cytotoxic Factor ◽  
Human Umbilical Vein ◽  
Induced Hypertension

1. Pregnancy-induced hypertension (or pre-eclampsia) is characterized by vasoconstriction, platelet aggregation and altered capillary permeability, implying disordered endothelial function and/or structure. Serum from women with pregnancy-induced hypertension has been reported by others to be cytotoxic to endothelial cells in vitro. We hypothesized that such serum contains a factor that limits the ability of endothelial cells to produce and/ or release prostacyclin. 2. Prostacyclin production by intact and damaged cultured human umbilical vein endothelial cells was measured after incubating these cells with serum from non-pregnant and normal pregnant women and women with pregnancy-induced hypertension. Confluent human umbilical vein endothelial cell monolayers (intact and damaged) were incubated with sera for 24 h at 37°C followed by 1 h of incubation with added thrombin (stimulated production) or media (basal production). Supernatants were then collected for measurement of 6-keto-prostaglandin F1α by radioimmunoassay. 3. Basal production of 6-keto-prostaglandin F1α was greater in response to serum from non-pregnant women than to that from pregnant women. Within each group, sub-lethally damaged cells had a similar basal production of 6-keto-prostaglandin F1α to that of intact cells. 4. Basal production of 6-keto-prostaglandin F1α by intact or damaged cells incubated with sera from normal pregnant women and from women with pregnancy-induced hypertension was similar. 5. In all groups the addition of thrombin to intact endothelial cells increased 6-keto-prostaglandin F1α production approximately 15–30-fold over basal levels, but only three- to five-fold in damaged endothelial cells. Stimulated production of 6-keto-prostaglandin F1α by intact or damaged cells was similar with sera from normal pregnant women and women with pregnancy-induced hypertension. 6. These results indicate that any cytotoxic factor present in the sera of women with pregnancy-induced hypertension is unlikely to act by reducing basal endothelial production of prostacyclin. Secondly, if endothelial cell injury occurs in these women they may have a reduced capacity to increase endothelial production of prostacyclin in response to thrombin and possibly other important physiological stimuli.

Serum from healthy pregnant women reduces oxidative stress in human umbilical vein endothelial cells

2002 ◽  
Vol 103 (1) ◽  
pp. 53-57 ◽  
Author(s):  
Fortunato SCALERA ◽  
Tina FISCHER ◽  
Dietmar SCHLEMBACH ◽  
Ernst BEINDER
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Pregnant Women ◽  
Reduced Glutathione ◽  
Umbilical Vein ◽  
Lipid Peroxides ◽  
Human Endothelial Cells ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

This study was conducted to compare the effects of serum from healthy pregnant women and that from pregnant women with pre-eclampsia on oxidative stress in endothelial cells in culture. Human umbilical vein endothelial cells (HUVECs) were incubated with serum from 18 pre-eclamptic, 18 healthy pregnant and 18 healthy non-pregnant women for 24h. The levels of reduced glutathione (GSH) and lipid peroxides (LPOs) were measured in endothelial cell lysates. Measurement of malondialdehyde in combination with 4-hydroxyalkenals has been used as an indicator of LPOs. Serum from healthy pregnant women decreased significantly the LPO content in HUVECs in comparison with serum from pre-eclamptic women and healthy non-pregnant women (30.7±6.6 compared with 39.3±10.9 and 41.0±12.7pmol/mg of protein respectively; P<0.003 and P<0.01 respectively). No differences in GSH content between the three groups (18.3±2.1nmol/mg of protein for healthy pregnant, 19.2±3.3nmol/mg for pre-eclamptic and 18.3±2.0nmol/mg for healthy non-pregnant women) were found. Thus serum from normal pregnant women contains a factor(s) that decreases oxidative stress in human endothelial cells. This mechanism might be altered in pre-eclampsia.

Circulating miR-3656 induces human umbilical vein endothelial cell injury by targeting eNOS and ADAMTS13

2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Jikang Shi ◽  
Yaxuan Ren ◽  
Sainan Liu ◽  
Qian Zhao ◽  
Fei Kong ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Injury ◽  
Umbilical Vein ◽  
Endothelial Cell Injury ◽  
Human Umbilical Vein

Curculigoside attenuates human umbilical vein endothelial cell injury induced by H2O2

2010 ◽  
Vol 132 (1) ◽  
pp. 233-239 ◽  
Author(s):  
Yun Kai Wang ◽  
Ya Jun Hong ◽  
Mao Wei ◽  
Ye Wu ◽  
Zhao Quan Huang ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Injury ◽  
Umbilical Vein ◽  
Endothelial Cell Injury ◽  
Human Umbilical Vein

THE LUPUS ANTICOAGULANT DOES NOT INHIBIT THE RELEASE OF PROSTACYCLIN FROM HUMAN ENDOTHELIAL CELLS

1987 ◽  
Author(s):  
W Petraiuolo ◽  
E Bovill ◽  
J Hoak
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Causal Relationship ◽  
Lupus Anticoagulant ◽  
Umbilical Vein ◽  
Human Endothelial Cells ◽  
Human Umbilical Vein ◽  
Blood Institute ◽  
Specialized Center ◽  
National Heart Lung

Decreased endothelial cell production of prostacyclin (PGI2) in response to the lupus anticoagulant has been previously demonstrated, and postulated to have a causal relationship to the thrombotic events associated with the lupus anticoagulant. Five patients who exhibited the anticoagulant were studied in an effort to determine if a relationship exists between exposure of endothelial cells to the lupus anticoagulant and decreased production of prostacyclin (PGI2). Human endothelial cells derived from human umbilical vein grown in culture were exposed to IgG fractions of patient plasmas containing the lupus anticoagulant. The amount of PGI2 released was determined by radioimmunoassay for 6-keto-PGF-l-alpha. The average PGI2 release in the controls was 20.6 picomol/500,000 endothelial cells, whereas those cells exposed to the lupus anticoagulant had a range of 25 to 114 picmol/500,000 cells. We were unable to demonstrate inhibition of the release of PGI2 by human endothelial cells, following exposure to the lupus anticoagulant.(Supported by NIH Grant HL 33723-2 and a Specialized Center of Research in Thrombosis Award HL 35058-01 from the National Heart, Lung and Blood Institute.)

scholarly journals Omentin-1 Ameliorated Free Fatty Acid-Induced Impairment in Proliferation, Migration, and Inflammatory States of HUVECs

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Yubin Chen ◽  
Fen Liu ◽  
Fei Han ◽  
Lizhi Lv ◽  
Can-e Tang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Fatty Acid ◽  
Endothelial Cell ◽  
Free Fatty Acid ◽  
Cell Injury ◽  
Umbilical Vein ◽  
Quantitative Polymerase Chain Reaction ◽  
Cell Counting ◽  
Endothelial Cell Injury ◽  
Umbilical Vein Endothelial Cells

Objectives. Endothelial cell injury is a critical pathological change during the development of atherosclerosis. Here, we explored the effect of omentin-1 on free fatty acid- (FFA-) induced endothelial cell injury. Methods. An FFA-induced endothelial cell injury model was established to investigate the role of omentin-1 in this process. Cell proliferation was analyzed with the Cell Counting Kit assay and flow cytometry. Scratch and transwell assays were used to evaluate cell migration. Factors secreted by endothelial cells after injury were detected by western blotting, reverse-transcription quantitative polymerase chain reaction, and cellular fluorescence assay. Results. Omentin-1 rescued the FFA-induced impaired proliferation and migration capabilities of human umbilical vein endothelial cells (HUVECs). It decreased the number of THP-1 cells attached to HUVECs in response to injury and inhibited the FFA-induced proinflammatory state of HUVECs. Conclusion. Omentin-1 could partly ameliorate FFA-induced endothelial cell injury.

scholarly journals CTRP3 Protects against High Glucose-Induced Cell Injury in Human Umbilical Vein Endothelial Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Fang Wang ◽  
Linlin Zhao ◽  
Yingguang Shan ◽  
Ran Li ◽  
Guijun Qin
Keyword(s):  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
High Glucose ◽  
Cell Injury ◽  
Umbilical Vein ◽  
Cell Loss ◽  
Inflammatory Factors ◽  
Therapeutic Drug ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Aims. Inflammation was closely associated with diabetes-related endothelial dysfunction. C1q/tumor necrosis factor-related protein 3 (CTRP3) is a member of the CTRP family and can provide cardioprotection in many cardiovascular diseases via suppressing the production of inflammatory factors. However, the role of CTRP3 in high glucose- (HG-) related endothelial dysfunction remains unclear. This study evaluates the effects of CTRP3 on HG-induced cell inflammation and apoptosis. Materials and Methods. To prevent high glucose-induced cell injury, human umbilical vein endothelial cells (HUVECs) were pretreated with recombinant CTRP3 for 1 hour followed by normal glucose (5.5 mmol/l) or high glucose (33 mmol/l) treatment. After that, cell apoptosis and inflammatory factors were determined. Results. Our results demonstrated that CTRP3 mRNA and protein expression were significantly decreased after HG exposure in HUVECs. Recombinant human CTRP3 inhibited HG-induced accumulation of inflammatory factors and cell loss in HUVECs. CTRP3 treatment also increased the phosphorylation levels of protein kinase B (AKT/PKB) and the mammalian target of rapamycin (mTOR) in HUVECs. CTRP3 lost its inhibitory effects on HG-induced cell inflammation and apoptosis after AKT inhibition. Knockdown of endogenous CTRP3 in HUVECs resulted in increased inflammation and decreased cell viability in vitro. Conclusions. Taken together, these findings indicated that CTRP3 treatment blocked the accumulation of inflammatory factors and cell loss in HUVECs after HG exposure through the activation of AKT-mTOR signaling pathway. Thus, CTRP3 may be a potential therapeutic drug for the prevention of diabetes-related endothelial dysfunction.

MODULATION of PROSTACYCLIN PRODUCTION BY HUMAN UMBILICAL VEIN ENDOTHELIAL CELLS WITH ECGF/HEPARIN MEDIUM : ROLE OF CELLULAR DENSITY AT CONFLUENCE

1987 ◽  
Author(s):  
O BOUTHERIN-FALSON ◽  
N BLAES
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Umbilical Vein ◽  
Calf Serum ◽  
Lower Amount ◽  
Endothelial Cell Proliferation ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Prostacyclin (PGI2) is a major product of arachidonic acid metabolism in vascular endothelial cells. In addition to the role of exogenous agents, its production could be modulated by culture conditions : proliferative state, medium renewal, subcultivation... The use of endothelial cell growth factor (ECGF) associated with heparin has been shown to improve human endothelial cell proliferation. Here we report that human umbilical vein endothelial cells (HUVEC) grown in that medium produce less prostacyclin than without growth factor.HUVEC were cultured in RPMI-199 1:1 + 20% fetal calf serum, added or not with ECGF (Bovine hypothalamus extract BTI Cambridge, 24 ug/ml) and heparin (from porcine intestinal mucosa, Signa, 90 ug/ml). After 4 days in culture, medium was removed and replaced by Tyrode Hepes buffer and basal production was measured after 20 min. Cells were then submitted to 5 min thrombin to assess PGI2 production in stimulated conditions. PGI2 production was estimated by specific radioimmunoassay for 6 keto PGFjalpha. For each point, cell number in the culture was counted after Trypsin EDTA treatment. In the present study, cells grown in ECGF-heparin medium produce lower amount of PGI2, compared to heparin or control medium. This result was observed in both basal and stimulated conditions. For each medium (ECGF-heparin, heparin, control), correlations between PGI2 production per cell and log cell density were shown to be significantly negative.These observations suggest that ECGF effect on PGI2 production could be a consequence of its growth factor activity, notably by the fact that it leads to an endothelial monolayer made of more numerous cells. Since it is now suggested by a number of clinical observations that PGI2 is rather produced in pathological conditions, culture models showing a weak production of PGI2 appear in that connection doser to the physiological conditions.

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