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F Russo-Marie

Publications and source records attributed to F Russo-Marie.

At least 91 records · Page 5Linked to original sources
PubMed1988

Rapid purification of two lipocortin-like proteins from mice lung.

We have purified two proteins (40 kDa and 36 kDa) from mice lung by the method of calcium-precipitation/EGTA solubilization and then a separation on a high anion exchanger column (Mono Q HR 5/5. Pharmacia) with a gradient of NaCl. The two proteins were strong inhibitors of phospholipase A2 as assessed in vitro with porcine pancreatic phospholipase A2 and [3H]-oleic acid labeled E. Coli membranes as substrate. The 40 kDa protein had a pI of 5.8 and was found to be immunologically related to human recombinant lipocortin I. The 36 kDa protein had a pI of 4.7 and cross-reacted with a polyclonal antibody raised against a 32 kDa human lipocortin-like protein described in human blood mononuclear cells. We report here a rapid purification of two distinct lipocortin-like proteins from mice lung.

Animals↗
PubMed1988

Lipocortins.

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Animals↗
PubMed1988

Characterization of a polyacrylamide gel-induced granuloma in mice: involvement of arachidonate metabolites.

The injection of polyacrylamide gel (Bio Gel P-4, 200-400 mesh) into the subcutaneous area of mice, induced an inflammatory reaction which was characterized by the migration of leukocytes (mainly neutrophils) from the blood vessels towards the polyacrylamide gel. A rapid protein accumulation was observed during the migration of cells towards the inflamed site. Neutrophils released some pro-inflammatory lipids (prostaglandins, leukotriene B4) and lysozyme, these products were assayed in the granuloma exudate at various times of the granuloma formation. In our experimental inflammatory model, the results suggest that neutrophils that are attracted by the polyacrylamide gel produce eicosanoids and lysozyme, which could act synergistically to potentiate cell migration and protein accumulation in the inflamed site.

Acrylic Resins↗
PubMed1987

Purification and characterization of a 32-kDa phospholipase A2 inhibitory protein (lipocortin) from human peripheral blood mononuclear cells.

A 32-kDa protein was isolated from human monocytes after calcium precipitation and chromatography. The protein activity was assessed by the inhibition of soluble phospholipase A2 (PLA2). This in vitro inhibitory effect on phospholipases A2 was found only with negatively charged phospholipids. The protein was also able to inhibit cellular PLA2 in mouse thymocytes. The biochemical properties and amino acid composition strongly suggest that the protein shares similarities with endonexin. Using a neutralizing monoclonal antibody against rat lipocortin, we found a cross-reactivity with the 32-kDa protein. According to the biochemical and immunological properties, we propose to relate this PLA2 inhibitory protein from human monocytes to lipocortin.

Amino Acids↗
PubMed1987

Lipocortin inhibition of extracellular and intracellular phospholipases A2 is substrate concentration dependent.

Hydrolysis of Escherichia coli membrane phospholipids by pancreatic phospholipase A2 was inhibited by lipocortin from human monocytes in a substrate dependent manner. Inhibition was completely overcome at substrate concentrations above 250 microM. Lipocortin also inhibited partially purified preparations of two intracellular phospholipases A2 isolated from rat liver mitochondria and rat platelets when these enzymes were assayed at low micromolar concentrations of phosphatidylethanolamine. Inhibition gradually decreased with increasing substrate concentrations both for pancreatic and platelet phospholipase A2 and became completely abolished above 15 and 50 microM phosphatidylethanolamine, respectively.

Animals↗
PubMed1987

[Biological effects of SIN-1 in the vascular wall].

The biological effects of two vasodilatory drugs, SIN-1 (the active metabolite of molsidomine) and nitroglycerin were analysed in the arterial endothelium and vascular muscle. Both drugs induce the secretion of prostacyclin in endothelial cells in culture, but this secretion is short-lived and occurs for high doses of the two drugs (above 10(-5)M). These same drugs induce a dose-dependent relaxing effect on the smooth muscle contracted either by norepinephrine or 5-hydroxytryptamine with an ED50 of 5.10(-7)M. This relaxation is neither secondary to an endothelium-derived product nor to a cyclooxygenase or lipoxygenase-derived product.

Animals↗
PubMed1987

[Effects of SIN-1, a metabolite of molsidomine, on paf-acether-blood platelets interactions].

The metabolite of molsidomine, 3-morpholino-syndnonimine (SIN-1) is a vasodilator and an inhibitor of platelet activation induced by adenosine-5'-diphosphate (ADP), arachidonic acid (AA) and thrombin. We present the results of SIN-1 on platelet aggregation induced by paf-acether and on the biosynthesis of this mediator by washed rabbit platelets. SIN-1 inhibits submaximal platelet aggregation induced by 50 pM paf-acether. This inhibition is dose-dependent (SIN-1 IC50: 37 +/- 10 nM, n = 3). SIN-1 also inhibits submaximal aggregations induced by ADP (IC50: 13 +/- 11 nM) and AA (IC50: 26 +/- 12 nM) (n = 3-5). Finally, SIN-1 inhibits dose-dependently the formation of lyso paf-acether (the precursor of paf-acether) and of thromboxane A2, and AA freeing by thrombin-stimulated platelets. Thus SIN-1 has a wide spectrum activity on platelets. He is both capable of inhibiting platelet aggregation induced by all used agonists and to inhibit the formation of paf-acether and thromboxane A2, two powerful mediators of platelet aggregation.

Animals↗
PubMed1986

PAF-acether-induced synthesis of prostacyclin by human endothelial cells.

Platelet activating factor, 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine (PAF-acether) is a potent platelet-stimulating agent formed by most circulating cells. Added to cultured human endothelial cells, PAF-acether induced a dose-dependent synthesis of 6-keto-PGF1 alpha, the major stable metabolite of prostacyclin (PGI2), with a maximal effect at 100 nM, a concentration equivalent to that which aggregates human platelets. No release of von Willebrand factor (vWF) was noted under the same conditions. The poorly active PAF-acether analogue, methoxy-PAF failed to stimulate 6-keto-PFG1 alpha synthesis and the PAF-acether antagonists 48740 RP, BN 52021 and Ro 19-3704, prevented the stimulatory effect of PAF-acether. Methyl-carbamate-PAF, an equieffective analogue of PAF-acether on platelets, also stimulated 6-keto-PGF1 alpha production. After a first stimulation by PAF-acether or methyl-carbamate-PAF, no response was detected when endothelial cells were re-exposed to either agonist, indicating auto- and cross-desensitization as described for other cells. Since PAF-acether stimulated [3H]arachidonate release from pre-labelled endothelial cells, our results suggest that it stimulates phospholipase activity, which accounts for the increased PGI2 synthesis. The auto- and cross-desensitization between PAF-acether and methyl-carbamate-PAF, ineffectiveness of methoxy-PAF and inhibition by selective antagonists strongly suggest interaction with specific membrane receptors.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Effects of gluco- and antiglucocorticoids on renal and aortic prostaglandin synthesis.

The effects of glucocorticoid agonists RU 26988 (G) and dexamethasone (D) and antagonist RU 486 (AG) on aortic and renal prostaglandin (PG) production were studied in Wistar rats. Blood pressure increased in rats administered G (20 mg X kg-1 X day-1) during 1 or 3 days; such increase was prevented by AG (100 mg X kg-1 X day-1). Renal papillary PGE2 release was increased after a 3-day administration of G, and this was prevented by AG. Neither G nor AG altered basal 6-keto-PGF1 alpha aortic production. However, G inhibited and AG magnified the stimulatory effect of ionophore A 23187, added in vitro, on 6-keto-PGF1 alpha production; AG reversed G inhibition. In addition, AG alone (20 mg X kg-1 X day-1 X 3 days) enhanced the stimulatory effect of angiotensin II (10(-8) M), added in vitro, on 6-keto-PGF1 alpha release. In vitro studies were performed on renomedullary interstitial cells grown in culture; G and D depressed PGE2 production in a dose-dependent manner; AG at equimolar 10(-8) M concentration inhibited this effect. In conclusion, AG inhibits the effects of G on blood pressure and PG synthesis. G exerts strong depressor activity on in vitro PGE2 renal production, whereas in vivo effects are more complex. Endogenous G inhibits aortic prostacyclin production, an action unmasked by AG administration. Diminished stimulation of vascular prostacyclin synthesis may contribute to vascular hyperreactivity in G-induced hypertension.

Androstanols↗
PubMed1985

Effect of intracellular oxygen-free radicals on the formation of lipid derived mediators in rat renomedullary interstitial cells.

An intracellular generation of oxygen free radicals was induced by phenazine methosulfate (PMS) in rat renomedullary interstitial cells (RMIC) in culture. This response was associated with an increase in PGE2 and 15 HETE production. The synthesis of cyclooxygenase and lipoxygenase derivatives in PMS-treated cells was inhibited by indomethacin and NDGA respectively. Inhibitors of PLA2 such as mepacrine and dexamethasone were able to inhibit partially the PGE2 synthesis induced by PMS. The formation of lyso-platelet activating factor, a product of membrane-bound phospholipid, by a PLA2 catalyzed reaction was also stimulated in PMS-treated cells. Superoxide dismutase added to the incubation medium enhanced the PMS-dependent PGE2 synthesis whereas catalase decreased it, suggesting the involvement of H2O2 in this process. In addition, a depletion of soluble thiol groups was observed in PMS-treated cells. Treatment of RMIC by the thiol oxidative agent, diamide, mimicked the effect of PMS on PGE2 synthesis, whereas diamide did not increase the formation of lyso-PAF indicating its inability to stimulate PLA2. These results suggest that cyclooxygenase may be involved in this process, indeed added arachidonate, bypassing PLA2, enhanced PGE2 synthesis in PMS-treated cells further supporting the involvement of cyclooxygenase. In conclusion, generation of oxygen free radicals by PMS in RMIC enhanced the synthesis of lipid derived mediators. A decrease in the cellular thiol content is partially involved in cyclooxygenase activation but does not appear to be involved in PLA2 activation.

Animals↗
PubMed1985

The presence of lipocortin in human embryonic skin fibroblasts and its regulation by anti-inflammatory steroids.

Human embryonic skin fibroblasts in culture produce pro-inflammatory lipid mediators and all types of prostanoids. When these cells were treated with the anti-inflammatory steroid, dexamethasone, prostaglandin production was inhibited. This phenomenon required glucocorticoid receptor occupancy and mRNA and protein synthesis. The inhibitory effect was prevented by treating the cells with a monoclonal antibody, BF 26, raised against renocortin, a lipocortin-like protein formed in rat kidney medulla interstitial cells in culture. When the proteins present in the supernatants and the cell pellets derived from control and dexamethasone-treated cells were analyzed for their ability to inhibit phospholipase A2, four inhibitory peaks, at 45, 30, 15 kDa and one peak under 12 kDa, were found in the supernatants of control and dexamethasone-treated cells, whereas one single inhibitory peak at 15 kDa was found in the cell pellets. The antiphospholipase activity was much greater in dexamethasone-treated cells than in control cells. These results suggest that preformed lipocortin exists in human cells and that lipocortin is synthesized and released under glucocorticoid treatment.

Abortifacient Agents, Steroidal↗
PubMed1985

Desensitization to PAF-induced bronchoconstriction and to activation of alveolar macrophages by repeated inhalations of PAF in the guinea pig.

Guinea-pig alveolar macrophages are activated in the presence of PAF-acether (PAF), as shown by O2.- production, suggesting that these cells, abundant in the lungs, are involved in PAF-induced bronchoconstriction. Alveolar macrophages collected after in vivo desensitization to the bronchoconstrictor effect of PAF became refractory to it in vitro, whereas the O2.- production in response to f-met-leu-phe persisted, although it was diminished suggesting a partial cross-desensitization. A similar desensitization to PAF was also observed in alveolar macrophages in vitro, demonstrating a stimulus-specific process. This study suggests that alveolar macrophages may be involved in bronchoconstriction induced by aerosol of PAF.

Aerosols↗
PubMed1985

Possible non-involvement of lipoxygenase pathway in the cerebral blood flow decrease due to indomethacin.

Indomethacin (10n mg/kg i.p.) induced a marked decrease in local cerebral blood flow (l.CBF), which was measured in the frontal cortex of unanesthetized rats by the hydrogen clearance technique. Brain prostaglandins (PGD2, PGE2, PGF2 alpha,) and 6kPGF1 alpha the stable metabolite of prostacyclin, were significantly decreased. Treatments with inhibitors of lipoxygenase (BW 755C and nordihydroguaiaretic acid) and with FPL 55712, a leukotriene receptor antagonist, did not influence the effect of indomethacin on 1.CBF. The results suggest that the release of vasoconstrictory leukotrienes does not play a major role in the lowering of 1.CBF by indomethacin.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1985

Defective IFN-gamma production in the human neonate. II. Role of increased sensitivity to the suppressive effects of prostaglandin E.

Analysis of endogenous production and effects of exogenous addition of interleukin 2 (IL 2), leukotrienes (LT), and prostaglandin E (PGE) has been used to investigate the dysregulation responsible for impaired PHA-induced IFN-gamma secretion by cord blood leukocytes (CBL). The addition of LT or IL 2 could not reverse the IFN defect of CBL. The production of these two mediators was found to be normal in CBL cultures. CBL and control leukocytes from adult donors produced comparable amounts of PGE2. In contrast, sensitivity to the suppressive effects of PGE2 on IFN-gamma secretion was much higher with CBL than with control leukocytes. Treatment with indomethacin reversed the IFN-gamma defect with most CBL tested, and the addition of physiologic amounts of PGE2 to indomethacin-treated cultures resulted in a profound impairment of IFN-gamma production similar to that of untreated CBL cultures. Preincubation of CBL for 24 hr before PHA stimulation resulted in restoration of a normal sensitivity to exogenous PGE2, in parallel with correction of the IFN-gamma defect. Our observations suggest that the impairment of IFN-gamma secretion in neonates is not due to deficient amplification circuits, but is the consequence of an exaggerated cellular sensitivity to the suppressive effects of PGE produced endogenously in normal amounts.

Adult↗