Prostacyclin production by human endothelial and bovine smooth muscle cells in culture

Dejana, Elisabetta; Balconi, Giovanna; Castellarnau, Conxita de; Barbieri, B; Vergara-Dauden, M.; Gaetano, Giovanni de

doi:10.1016/0005-2760(83)90027-9

Cited by 47 publications

(4 citation statements)

References 13 publications

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“…2 The cells were used at the first passage at confluence, and they were maintained at 37°C in a water-saturated atmosphere at 95% air/5% CO 2 and fed twice a week. EC were routinely characterized by indirect immunofluorescence with rabbit anti-human von Willebrand factor antibodies (Behringwerke AG, Marburg, FRG).…”

Section: Endothelial Cell Culturementioning

confidence: 99%

“…AA was prepared and stored as described previously. 2 At the end of this period, the supernatant was removed, and the 6-keto-PGF 1a content was measured.…”

Section: Endothelial Cell Stimulation With Lnterleukin-1mentioning

confidence: 99%

“…These cells were prepared and stored as described 2 for 30 minutes at 37°C. At the end of the incubation, the aspirin was removed, the cells were washed twice with 2 ml of PBS, and then they were cultured in the presence or absence of 10 U/ml of IL-1.…”

Section: Aspirin Treatment Of Endothelial Cellsmentioning

confidence: 99%

“…2 ' 3 We and other groups have shown that the immunomediator, interieukin-1 (IL-1), has a peculiar way of inducing PGI 2 synthesis in EC. 45 IL-1 stimulation requires a few hours to become apparent, but then it lasts for several hours.…”

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Interleukin-1 stimulates prostacyclin production by cultured human endothelial cells by increasing arachidonic acid mobilization and conversion.

et al. 1990

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lnterieukln-1 (IL-1) induced slow, lasting activation of human endothelial cells (EC) to release prostacyclin (PGI 2 ). This was accompanied by endogenous3 H-arachldonlc acid f H-AA) release and by a time-dependent Increase In the cells' ability to convert exogenous AA. The continuous presence of IL-1 was not required, but about a 1-hour stimulation with the cytoklne was sufficient to trigger the cells to synthesize PGI 2 for several hours. The spectrum of 3 H-AA conversion shows that, In addition to 6-ketoprostaglandln F 1a , prostaglandln F^, also was raised after IL-1. The recovery of PGI 2 synthesis after aspirin was faster In IL-1-treated EC than In control cells. These data define some of the characteristics of IL-1 stimulation of PGI 2 and suggest that this process Is mediated both by endogenous AA mobilization and by an increase In cyclooxygenase activity. (Arteriosclerosis 10:129-134, January/February 1990) P rostacyclin (PGy is an important biosynthetic product of endothelial cells (EC). It inhibits platelet aggregation and thrombus formation and acts as a potent vasodilator by causing relaxation in vascular smooth muscle cells.1 PGI 2 hatf-life, when released into the circulation, is in the range of a few minutes, and its activity on platelets and vascular tone is extremely short lived. 1 Therefore, its biological relevance in vivo is strictly related to "how much and for how long" it can be produced by the vessel wall.Most known activators, e.g., thrombin, bradykinin, or ionophore A23187, induce a very fast, short-lasting release of PGI 2 by EC, followed by cell refractoriness to subsequent stimulation.2 ' 3 We and other groups have shown that the immunomediator, interieukin-1 (IL-1), has a peculiar way of inducing PGI 2 synthesis in EC.45 IL-1 stimulation requires a few hours to become apparent, but then it lasts for several hours.IL-1 is probably one of the most important mediators of the hemodynamic and hematological changes characteristic of septic shock.6 ' 7 The hemodynamic alterations, particularly the hypotension caused by IL-1, require cyclooxygenase products, since they are reversed by inhibitors of this enzyme.7 It has, therefore, been hypothesized that PGI 2 synthesis by EC plays an important role in mediating the slow and lasting drop in systemic vascular resistance that follows IL-1 release in the circulation. Despite its biological importance, little is known about the mechanism and the pattern through which IL-1 exerts its stimulatory activity on EC. In this work, we report that IL-1 induces endogenous arachidonic add (AA) mobilization and increases its conversion to prostaglandins via an increase in cyclooxygenase synthesis and activity. This effect is long lasting but does not need the continuous presence of IL-1 to be apparent. Methods Endothelial Cell CultureEC were isolated from human umbilical vein and cultured in medium 199 supplemented with 20% newborn calf serum as previously described in detail.2 The cells were used at the first passage at confluence, and they were maintaine...

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Section: Endothelial Cell Culturementioning

confidence: 99%

“…AA was prepared and stored as described previously. 2 At the end of this period, the supernatant was removed, and the 6-keto-PGF 1a content was measured.…”

Section: Endothelial Cell Stimulation With Lnterleukin-1mentioning

confidence: 99%

Section: Aspirin Treatment Of Endothelial Cellsmentioning

confidence: 99%

mentioning

confidence: 99%

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Interleukin-1 stimulates prostacyclin production by cultured human endothelial cells by increasing arachidonic acid mobilization and conversion.

et al. 1990

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Lipid transfer between endothelial and smooth muscle cells in coculture

Stoll

Spector

1987

Journal Cellular Physiology

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A coculture system was employed to study the interactions between endothelium and vascular smooth muscle cells in arachidonic acid metabolism. Bovine aortic endothelial cells grown on micropore filters impregnated with gelatin and coated with fibronectin are mounted on polystyrene chambers and suspended over confluent smooth muscle cultures. The endothelial basal laminae are oriented toward the underlying smooth muscle, and the two layers are separated by only 1 mm. Each cell layer was assayed individually: apical and basolateral fluid also was collected separately for assay. Fatty acids, including arachidonic acid, are readily transferred between the endothelial and smooth muscle cells in this system. Distribution of the incorporated fatty acids among the lipids of each cell is the same as when the fatty acid is added directly to the culture medium. Arachidonic acid released from endothelial cells is available as a substrate for prostaglandin production by smooth muscle. In addition, fatty acids released from the smooth muscle cells can pass through the endothelium and accumulate in the fluid bathing the endothelial apical surface. These fatty acid interchanges may be involved in cell-cell signaling within the vascular wall, the clearance of lipids from the vascular wall, or the redistribution of arachidonic acid and other polyunsaturated fatty acids between adjacent cell types. Furthermore, the findings suggest that prostaglandin production by smooth muscle cells can occur in response to stimuli that cause arachidonic acid release from endothelial cells.

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Arachidonic Acid Inhibits Cysteinyl-Leukotriene Receptor Activation in Human Pulmonary Vessels

Walch

Norel

Gascard

et al. 2003

Advances in Experimental Medicine and Biology

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Prostacyclin production by human endothelial and bovine smooth muscle cells in culture

Cited by 47 publications

References 13 publications

Interleukin-1 stimulates prostacyclin production by cultured human endothelial cells by increasing arachidonic acid mobilization and conversion.

Interleukin-1 stimulates prostacyclin production by cultured human endothelial cells by increasing arachidonic acid mobilization and conversion.

Lipid transfer between endothelial and smooth muscle cells in coculture

Arachidonic Acid Inhibits Cysteinyl-Leukotriene Receptor Activation in Human Pulmonary Vessels

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