Stimulation of Prostacyclin Production in Cultured Pulmonary Artery Endothelial Cells by Pseudomonas Aeruginosa Cytotoxin: Membrane Attack and Calcium Influx

2015 ◽  
pp. 89-93
Author(s):  
N. Suttorp ◽  
W. Seeger ◽  
J. Uhl ◽  
F. Lutz ◽  
L. Roka
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Endothelial Cells ◽  
Pulmonary Artery ◽  
Calcium Influx ◽  
Prostacyclin Production ◽  
Stimulation Of

scholarly journals Thrombin-mediated increases in cytosolic [Ca2+] involve different mechanisms in human pulmonary artery smooth muscle and endothelial cells

2008 ◽  
Vol 295 (6) ◽  
pp. L1048-L1055 ◽  
Author(s):  
Richard S. Sacks ◽  
Amy L. Firth ◽  
Carmelle V. Remillard ◽  
Negin Agange ◽  
Jocelyn Yau ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Calcium Influx ◽  
Dynamic Balance ◽  
Cyclopiazonic Acid ◽  
Cell Types ◽  
Intracellular Ca ◽  
Pulmonary Artery Smooth Muscle ◽  
Human Pulmonary Artery

Thrombin is a procoagulant inflammatory agonist that can disrupt the endothelium-lumen barrier in the lung by causing contraction of endothelial cells and promote pulmonary cell proliferation. Both contraction and proliferation require increases in cytosolic Ca2+ concentration ([Ca2+]cyt). In this study, we compared the effect of thrombin on Ca2+ signaling in human pulmonary artery smooth muscle (PASMC) and endothelial (PAEC) cells. Thrombin increased the [Ca2+]cyt in both cell types; however, the transient response was significantly higher and recovered quicker in the PASMC, suggesting different mechanisms may contribute to thrombin-mediated increases in [Ca2+]cyt in these cell types. Depletion of intracellular stores with cyclopiazonic acid (CPA) in the absence of extracellular Ca2+ induced calcium transients representative of those observed in response to thrombin in both cell types. Interestingly, CPA pretreatment significantly attenuated thrombin-induced Ca2+ release in PASMC; this attenuation was not apparent in PAEC, indicating that a PAEC-specific mechanism was targeted by thrombin. Treatment with a combination of CPA, caffeine, and ryanodine also failed to abolish the thrombin-induced Ca2+ transient in PAEC. Notably, thrombin-induced receptor-mediated calcium influx was still observed in PASMC after CPA pretreatment in the presence of extracellular Ca2+. Ca2+ oscillations were triggered by thrombin in PASMC resulting from a balance of extracellular Ca2+ influx and Ca2+ reuptake by the sarcoplasmic reticulum. The data show that thrombin induces increases in intracellular calcium in PASMC and PAEC with a distinct CPA-, caffeine-, and ryanodine-insensitive release existing only in PAEC. Furthermore, a dynamic balance between Ca2+ influx, intracellular Ca2+ release, and reuptake underlie the Ca2+ transients evoked by thrombin in some PASMC. Understanding of such mechanisms will provide an important insight into thrombin-mediated vascular injury during hypertension.

Stimulation of proteoglycans by IGF I and II in microvessel and large vessel endothelial cells

1987 ◽  
Vol 253 (1) ◽  
pp. E21-E27
Author(s):  
R. S. Bar ◽  
B. L. Dake ◽  
S. Stueck
Keyword(s):  
Endothelial Cells ◽  
Pulmonary Artery ◽  
Vascular Endothelial Cells ◽  
Pulmonary Arteries ◽  
Large Vessel ◽  
Dependent Manner ◽  
Disease States ◽  
Igf I ◽  
Stimulation Of

Endothelial cells were cultured from bovine capillaries and pulmonary arteries, and the effect of insulinlike growth factor (IGF) I and II (multiplication-stimulating activity) and insulin on the synthesis of proteoglycans was determined. IGF I and II stimulated 35SO4 incorporation into proteoglycans in a dose-dependent manner in both microvessel and pulmonary artery endothelial cells with maximum threefold increases. In pulmonary artery cells, the IGFs caused a general stimulation of all classes of glycosaminoglycan-containing proteoglycans. In microvessel endothelial cells, the IGFs appeared to preferentially increase heparan sulfate-containing proteoglycans. Insulin, at concentrations up to 10(-6) M, had no effect on the synthesis of proteoglycans in either microvessel or pulmonary arterial endothelial cells. Thus, the IGFs stimulate the synthesis of proteoglycans in both microvessel and large vessel endothelial cells, a property that is not mimicked by insulin. Because vascular endothelial cells are bathed by IGFs in vivo, such IGF-mediated functions are likely to be significant in both the normal physiology of vascular endothelium and in disease states such as diabetes mellitus.

Serotonin uptake by bovine pulmonary artery endothelial cells in culture. II. Stimulation by hypoxia

1986 ◽  
Vol 250 (5) ◽  
pp. C766-C770 ◽  
Author(s):  
S. L. Lee ◽  
B. L. Fanburg
Keyword(s):  
Endothelial Cells ◽  
Pulmonary Artery ◽  
Cell Number ◽  
Morphological Evidence ◽  
Monoamine Oxidase Activity ◽  
Trypan Blue Exclusion ◽  
Cells In Culture ◽  
Low Concentrations ◽  
5 Ht Uptake ◽  
Stimulation Of

Exposure of bovine pulmonary artery endothelial cells to 3% O2 resulted in approximately twofold stimulation of serotonin (5-HT) uptake after 24-48 h when compared with cells exposed to 20% O2. The enhanced uptake was reversed after 48 h when cells were again placed in 20% O2. The stimulation was not observed after 0.5 or 2 h of exposure to hypoxia. The stimulation was present when iproniazid blocked conversion of 5-HT to 5-hydroxyindole-3-acetic acid, indicating that enhanced uptake did not occur through augmentation of monoamine oxidase activity. Stimulation of uptake by hypoxia occurred at low concentrations of 5-HT (up to 10(-6) M) but not at high 5-HT concentrations (greater than 10(-5) M) and was blocked by imipramine or absence of sodium from the medium, indicating that high-affinity transport and not diffusion of 5-HT was stimulated. Furthermore, exposure of cells to hypoxia did not produce morphological evidence of injury or change in protein content or trypan blue exclusion. The cell number of 3% O2-exposed cells was slightly reduced when compared with controls after 48 h. There was no change in cellular ATP or increase in lactate dehydrogenase in medium of cells exposed to 3% O2. Thus exposure of endothelial cells in culture to hypoxia stimulates the membrane activity of 5-HT accumulation with no evidence of injury to the cell.

Modulation of mitochondrial Ca2+ by nitric oxide in cultured bovine vascular endothelial cells

2005 ◽  
Vol 289 (4) ◽  
pp. C836-C845 ◽  
Author(s):  
Elena N. Dedkova ◽  
Lothar A. Blatter
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Membrane Potential ◽  
Pulmonary Artery ◽  
Laser Scanning ◽  
Mitochondrial Permeability Transition ◽  
No Production ◽  
No Donor ◽  
Negative Feedback Regulation ◽  
Stimulation Of

In the present study, we used laser scanning confocal microscopy in combination with fluorescent indicator dyes to investigate the effects of nitric oxide (NO) produced endogenously by stimulation of the mitochondria-specific NO synthase (mtNOS) or applied exogenously through a NO donor, on mitochondrial Ca2+ uptake, membrane potential, and gating of mitochondrial permeability transition pore (PTP) in permeabilized cultured calf pulmonary artery endothelial (CPAE) cells. Higher concentrations (100–500 μM) of the NO donor spermine NONOate (Sper/NO) significantly reduced mitochondrial Ca2+ uptake and Ca2+ extrusion rates, whereas low concentrations of Sper/NO (<100 μM) had no effect on mitochondrial Ca2+ levels ([Ca2+]mt). Stimulation of mitochondrial NO production by incubating cells with 1 mM l-arginine also decreased mitochondrial Ca2+ uptake, whereas inhibition of mtNOS with 10 μM l- N5-(1-iminoethyl)ornithine resulted in a significant increase of [Ca2+]mt. Sper/NO application caused a dose-dependent sustained mitochondrial depolarization as revealed with the voltage-sensitive dye tetramethylrhodamine ethyl ester (TMRE). Blocking mtNOS hyperpolarized basal mitochondrial membrane potential and partially prevented Ca2+-induced decrease in TMRE fluorescence. Higher concentrations of Sper/NO (100–500 μM) induced PTP opening, whereas lower concentrations (<100 μM) had no effect. The data demonstrate that in calf pulmonary artery endothelial cells, stimulation of mitochondrial Ca2+ uptake can activate NO production in mitochondria that in turn can modulate mitochondrial Ca2+ uptake and efflux, demonstrating a negative feedback regulation. This mechanism may be particularly important to protect against mitochondrial Ca2+ overload under pathological conditions where cellular [NO] can reach very high levels.

Sign in / Sign up

Export Citation Format

Share Document