Characteristics of Cyclosporine Induction of Increased Prostaglandin Levels From Human Peripheral Blood Monocytes

Whisler, Ronald L.; Lindsey, Jenifer A.; Proctor, Katherine V. W.; Morisaki, Naho; Cornwell, David G.

doi:10.1097/00007890-198410000-00012

Cited by 52 publications

(19 citation statements)

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“…They postulated that this protec tive effect of ciclosporin A may be explained by a possible interrelationship between the cell immune system and the ischemia pro cess. Ciclosporin A appears to selectively in hibit helper T-lymphocyte proliferation in response to alloantigen presentation [27], in addition ciclosporin A has been reported to induce monocyte production of PgEs [28,29] which then reduces la expression on en dothelial cells, monocytes and macrophages. One interesting hypothesis is that ischemic injury may induce structural alterations in the membrane surface of hepatocytes and lead to activation of the immune system.…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Prostaglandin E<sub>1</sub>on Normothermic Liver Ischemia

Crafa¹,

Gugenheim²,

Saint–Paul

et al. 1991

Eur Surg Res

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Effects of treatment with prostaglandin E₁ (PgE₁) on normothermic liver ischemia were studied in male Lewis rats. Animals were subjected to 90 min of warm liver ischemia. Two groups of rats were constituted: group A (no treatment) and group B (PgE₁ treatment). PgE₁ (100 µg/kg) was given as a bolus 2 min before induction of ischemia and 2 min before the end of ischemia. Survival rates were assessed and, 6 h after the end of ischemia, serum transaminases, histology of the liver, Kupffer cell activity were evaluated. PgE₁ treatment significantly improved survival rate (80%) in comparison with the nontreated group (40%). A significant reduction in transaminase levels was observed after PgE₁ treatment. The extent of necrosis and congestion was improved by PgE₁ treatment. Sheep red blood cell ⁵¹Cr liver uptake was deeply depressed 6 h after the end of ischemia in group A (6 ± 2.3 %/g tissue), and was significantly higher (p < 0.001) after PgE₁ administration in group B (32.98 ± 11.7 %/g tissue). Our results demonstrate that PgE₁ is able to protect the liver from ischemic insult. The mechanism by which prostaglandins exert this beneficial effect on normothermic liver ischemia may be related to their action on hepatic macrophages.

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Section: Discussionmentioning

confidence: 99%

Protective Effects of Prostaglandin E<sub>1</sub>on Normothermic Liver Ischemia

Crafa¹,

Gugenheim²,

Saint–Paul

et al. 1991

Eur Surg Res

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“…Nonadherent cells were removed by rinsing with Seligmann's balanced salt solution/2% albumin, and adherent M0s were harvested with a rubber policeman. The adherent M0s were more than 90% pure by immunofluorescence analysis, were functionally intact as assessed by chemotaxis and phagocytosis, demonstrated 90% or more esterase activity, 19 - 34 and showed greater than 90% viability by trypan blue exclusion. In several experiments, adherent M0s were suspended in cloning medium (see "Smooth Muscle Cells" section in "Methods") or cloning medium containing 5 mM EDTA and incubated for 10 minutes to remove adherent platelets.…”

Section: Peripheral Blood Monocytesmentioning

confidence: 99%

“…19 - 33 Peripheral blood mononuclear cells were rinsed twice in Seligmann's balanced salt solution containing 2% human albumin and resuspended at 10 7 cells/ml in RPMI 1640 supplemented with 10% fetal bovine serum. Then 5 ml of the cell suspension was added to a 100-mm-diameter plastic Petri dish (No.…”

Section: Peripheral Blood Monocytesmentioning

confidence: 99%

Interactions between the monocyte/macrophage and the vascular smooth muscle cell. Stimulation of mitogenesis by a soluble factor and of prostanoid synthesis by cell-cell contact.

Zhang

Downs

Lindsey

et al. 1993

Arterioscler Thromb

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The effect of soluble factors from the monocyte/macrophage (M0) on cell proliferation and the functional effects of cell-cell contact on the arachidonic acid (AA) cascade were studied with vascular smooth muscle cells (SMCs). Peripheral blood M0s were isolated by adherence or in a Percoll gradient, and alveolar M0s were obtained by lavage. Conditioned medium (CM) was prepared by preincubating M0s with medium alone or by separating SMC and M0 cocultures by a membrane insert Cell proliferation (image analysis) and 6-ketoprostaglandin F 1

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“…However, some other in vitro studies have reported that CsA can enhance the excretion of prostaglandin E2 and tromboxane, mediators of osteoclastic bone resorption (Whisler et al, 1984;Esa et al, 1988).…”

Section: Introductionmentioning

confidence: 99%

The Effect of Cyclosporin A on Alveolar Bone in Rats Subjected to Experimental Periodontal Disease

et al. 2006

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Cyclosporine A (CsA), broadly used in organ transplantation, may contribute to pathogenesis of osteoporosis. The aim of this study was to investigate the effects of CsA on alveolar bone in rats subjected or not to experimental periodontal disease using biochemical, radiographic, and histometric analysis. Forty Wistar rats were divided into 4 equal groups: Group I (Control), Group II (CsA was injected subcutaneously in a daily dose of 10 mg/kg), Group III (Ligature was placed around the mandibular molars), Group IV (Ligature+CsA). After 60 days, rats were decapitated, serum alkaline phosphatase and calcium levels were measured. Radiographic-alveolar bone loss (ABL), histometric-ABL, and percentage of new alveolar bone formation (NABF%) were determined on mandibular molars. Significant increase in serum alkaline phosphatase levels ( p < 0.001), no significant difference in calcium levels were observed ( p > 0.05) in Group IV compared to Group III. Radiographic and histometric-ABL were significantly less ( p < 0.001), NABF% was significantly greater ( p < 0.05) in Group IV than in Group III. No significant difference in any of the parameters between Group II and Group I was found. It can be concluded that in the presence of periodontal disease, CsA treatment may bring out an imbalance in the alveolar bone homeostasis by decreasing resorption and stimulating formation of alveolar bone in rats.

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Characteristics of Cyclosporine Induction of Increased Prostaglandin Levels From Human Peripheral Blood Monocytes

Cited by 52 publications

References 0 publications

Protective Effects of Prostaglandin E<sub>1</sub>on Normothermic Liver Ischemia

Protective Effects of Prostaglandin E<sub>1</sub>on Normothermic Liver Ischemia

Interactions between the monocyte/macrophage and the vascular smooth muscle cell. Stimulation of mitogenesis by a soluble factor and of prostanoid synthesis by cell-cell contact.

The Effect of Cyclosporin A on Alveolar Bone in Rats Subjected to Experimental Periodontal Disease

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