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F Russo-Marie

Publications and source records attributed to F Russo-Marie.

123 records · Page 7Linked to original sources
PubMed1981

Prostaglandin secretion by human thymic epithelium: in vitro effects of steroids.

Increasing evidence suggests a role for prostaglandins in the immune response. As steroids have been shown recently to modulate prostaglandin secretion, we have studied the secretion of prostaglandin and the effect of various steroids in culture of human thymus epithelial cells. Using reverse phase high pressure liquid chromatography and radioimmunoassays, we have shown that these cells produce substantial amounts of PGE2 and PGF2 alpha and that this secretion is modulated by steroid hormones. Prostaglandin could represent one of the factors of the thymic environment which respond to steroid hormones.

Cells, Cultured↗
PubMed1980

[Effect of steroid hormones on the secretion of prostaglandins by human thymic epithelial cells in culture].

Increasing evidence suggests a role of prostaglandins in the immune response. As steroids have been shown recently to modulate prostaglandin secretion, we have studied the secretion of prostaglandin and the effect of various steroids in cultures of human thymus epithelial cells. Using thin layer chromatography and radioimmunoassays, we have shown that these cells produce substantial amounts of PGE2 and PGF2 alpha and that this secretion is modulated by steroid hormones. We therefore suggest that prostaglandin could represent one of the factors of the thymic environment involved in lymphocyte maturation, which respond to steroid hormones.

Cells, Cultured↗
PubMed1980

Effect of dexamethasone on cyclo-oxygenase activity in reno-medullary cells in culture.

The steroid-induced inhibition of prostaglandin secretion has been shown to be mediated through the interaction of the steroid with specific receptors and to require RNA and protein synthesis. At present the nature of the protein(s) involved is unknown although several suggestions have been made for the role of phospholipase A2. It has also been postulated that the early action of steroid is a stimulation of cyclo-oxygenase activity leading only secondarily to an inhibition of arachidonate supply. In this paper, we have therefore investigated the effect of dexamethasone on cyclo-oxygenase activity in cultures of rat reno-medullary interstitial cells. Pretreatment of the cells with the anti-inflammatory steroid dexamethasone induces a moderate increase in cyclo-oxygenase activity but this elevation does not appear sufficient to account for the inhibitory action of dexamethasone on PG secretion.

Animals↗
PubMed1979

Prostaglandin synthesis by isolated rat renal glomeruli.

The PGE2, PGF2 alpha and 6-keto-PGF1 alpha contents of the incubation medium of glomeruli isolated from rat kidney were measured at different times with or without addition of arachidonic acid. These prostaglandins accumulated progressively with time and reached equilibrium after 60--120 min incubation. Synthesis of the 3 prostaglandins was inhibited when indomethacin was added whereas it was markedly enhanced, mainly for PGE2, at increasing doses of arachidonic acid. Plateaus were reached above 5 micrograms/ml and concentrations corresponding to 50% of the maximum values were 2 micrograms/ml for PGE2 and PGF2 alpha, and 0.8 microgram/ml for 6-keto-PGF1 alpha. There were strictly linear relationships between PGE2 or PGF2 alpha productions and the concentration of glomerular protein. PGE2 and PGF2 alpha synthesis with or without arachidonic acid were maximum at 30--37 degrees C. PGE2 glomerular content was almost undetectable initially and increased with time. These data demonstrate that PGE2, PGF2 alpha and PGI2, in order of decreasing abundance, are synthesized by the glomerular cells and suggest that PGE2 and PGI2-sensitive glomerular adenylate cyclase activities and PGE2-sensitive renin synthesis may be stimulated by prostaglandins formed in the glomeruli themselves.

Animals↗
PubMed1979

Mechanism of glucocorticoid-induced inhibition of prostaglandin synthesis.

In order to study the mechanism of steroid-induced inhibition of prostaglandin (PG) secretion, we have used rat renomedullary interstitial cells grown in tissue culture as an in vitro model. These cells have been shown by radio-immunoassay to produce high amounts of prostaglandins, mainly PGE2 and PGF2 alpha. Using (3H) dexamethasone, we have demonstrated in our cultures the existence of glucocorticoid binding sites which exhibit all the characteristics of physiological glucocorticoid receptors. Comparison between the biological activity (i.e. the ability to inhibit PG secretion) of the various steroids tested (dexamethasone, corticosterone, aldosterone, progesterone and estradiol) and their affinities for the glucocorticoid binding sites reveals a striking correlation between these two parameters. Steroids which bind to the receptors also inhibit prostaglandin secretion whereas testosterone and estradiol, which have a very weak affinity for the glucocorticoid binding sites do not inhibit PG secretion. In addition, actinomycin D (0.1 microgram/ml) and cycloheximide (0.1 microgram/ml) are able to abolish the inhibitory effect of dexamethasone on PG secretion. Our results indicate that the action of corticosteroids on prostaglandin secretion, which is believed to be the basis of their anti-inflammatory properties, is mediated through receptor occupancy and requires RNA and protein synthesis.

Animals↗
PubMed1976

Effects of haemodialysis on fractional intestinal absorption of calcium in uraemia.

Fractional intestinal absorption of calcium was measured in 41 haemodialysed patients 4 hours after an oral dose of 47 Ca. Fractional intestinal calcium absorption was 40.3 +/- 1.9% (SEM) when measured 10 to 12 hours after a haemodialysis session (dialysate calcium concentration: 1.75 mmol/litre). This value was significantly lower (p less than 0.001) than that in 26 healthy controls (56.8 +/- 1.8%) and higher (p less than 0.05) than that of 35 patients with chronic renal failure treated conservatively (34.5 +/- 2.1%). In 17 patients, fractional intestinal calcium absorption was measured just before and just after a dialysis session. Pre-dialysis fractional intestinal calcium absorption (33.7 +/- 3.0%) was not significantly different from fractional intestinal calcium absorption in uraemic patients treated conservatively, while after dialysis fractional intestinal calcium absorption had increased significantly to 42.0 +/- 2.6% (p less than 0.001). It is suggested that the transient increase in fractional intestinal calcium absorption observed after dialysis could be related to dialysis induced volume depletion rather than to a vitamin D-dependent mechanism.

Calcium↗
PubMedDate not supplied

Platelet activation--a role for a 40K anti-phospholipase A2 protein indistinguishable from lipocortin.

Stimulus-response (S-R) coupling in platelets requires an intermediary other than an elevation in cytosolic free calcium ([Ca2+]i). While an increase in [Ca2+]i is essential in S-R coupling, effecting phosphorylation of myosin of relative molecular mass (Mr) 20,000 (20 K), platelet activation is also associated with phosphorylation of a 40K protein, which can occur in the absence of changes in [Ca2+]i. The 40K protein is the substrate for protein kinase C (PKC). Mounting evidence suggests that activation of PKC by diacylglycerol is the other signal involved in S-R coupling. Although phosphorylation of the 40K protein is associated with certain platelet functional responses, no precise role has been accredited to it. Recently, we and others have described several proteins (collectively known as lipocortin) which inhibit phospholipase A2 (PLA2). One of the most conspicuous proteins of this group is a 40K peptide whose inhibitory activity can be suppressed by prior phosphorylation. We hypothesized that the 40K protein described in platelets may possess anti-PLA2 activity and that phosphorylation by PKC, suppressing its inhibitory activity, may represent the mechanism underlying mobilization of arachidonic acid, the precursor of prostaglandins. The results of the present study strongly support this hypothesis.

Alkaline Phosphatase↗
PubMedDate not supplied

[Current data on lipocortins].

Lipocortins, recently renamed annexins belong to a recently described family of intracellular proteins. Their main property is to bind negatively charged phospholipids in the presence of calcium. If lipocortins are added exogenously onto cells in vitro models or in vivo to the whole animal, they possess anti-inflammatory as well as anti-coagulant properties. Their intracellular function is unknown, nevertheless, it is possible that they may interact with some functions of membrane proteins, enzymes or other proteins as a consequence of their binding to cell membranes.

Animals↗