Pregnancy-induced hypertension decreases Kv1.3 potassium channel expression and function in human umbilical vein smooth muscle

2020 ◽  
Vol 882 ◽  
pp. 173281 ◽  
Author(s):  
Vladimir Djokic ◽  
Svetlana Jankovic ◽  
Milica Labudovic-Borovic ◽  
Jelena Rakocevic ◽  
Jelena Stanisic ◽  
...  
1992 ◽  
Vol 82 (4) ◽  
pp. 383-388 ◽  
Author(s):  
Vivienne C. Zammit ◽  
Judith A. Whitworth ◽  
Mark A. Brown

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.


2015 ◽  
Vol 3 (44) ◽  
pp. 8717-8728 ◽  
Author(s):  
Xin Li ◽  
Shuheng Yuan ◽  
Si Chen ◽  
Rifang Luo ◽  
Kaiqin Xiong ◽  
...  

An angiopoietin-1 functionalized surface was establishedviapolydopamine coating and regulated HUVECs survival, proliferation and function.


1998 ◽  
Vol 275 (4) ◽  
pp. C1031-C1039 ◽  
Author(s):  
Ilia Voskoboinik ◽  
Karin Söderholm ◽  
Ian A. Cotgreave

Human umbilical vein smooth muscle cells (HUVSMCs) utilize extracellular cystine, glutathione (GSH), and N-acetylcysteine (NAC) to synthesize cellular GSH. Extracellular cystine was effective from 5 μM, whereas GSH and NAC were required at 100 μM for comparable effects. The efficacy of extracellular GSH was dependent on de novo GSH synthesis, indicating a dependence on cellular γ-glutamyltransferase (glutamyl transpeptidase). Coculture of syngenetic HUVSMCs and corresponding human umbilical vein endothelial cells (HUVECs) on porous supports restricted cystine- or GSH-stimulated synthesis of HUVSMC GSH when supplied on the “luminal” endothelial side. Thus HUVSMC GSH rapidly attained a steady-state level below that achieved in the absence of interposed HUVECs. HUVSMCs also readily utilize both reduced ascorbate (AA) and oxidized dehydroascorbate (DHAA) over the range 50–500 μM. Phloretin effectively blocked both AA- and DHAA-stimulated assimilation of intracellular AA, indicating a role for a glucose transporter in their transport. Uptake of extracellular AA was also sensitive to extracellular, but not intracellular, thiol depletion. When AA was applied to the endothelial side of the coculture model, assimilation of intracellular AA in HUVSMCs was restricted to a steady-state level below that achieved by free access.


Channels ◽  
2017 ◽  
Vol 11 (4) ◽  
pp. 305-315 ◽  
Author(s):  
Hai M. Nguyen ◽  
Linda V. Blomster ◽  
Palle Christophersen ◽  
Heike Wulff

1998 ◽  
Vol 60 (1) ◽  
pp. 13-17 ◽  
Author(s):  
Roland Walter ◽  
Philippe Linscheid ◽  
Nenad Blau ◽  
Lucja Kierat ◽  
Andreas Schaffner ◽  
...  

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