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Biomedical subjects

B Perret

Publications and source records attributed to B Perret.

71 records · Page 4Linked to original sources
PubMed1987

High density lipoprotein and low density lipoprotein utilization by human granulosa cells for progesterone synthesis in serum-free culture: respective contributions of free and esterified cholesterol.

Human preovulatory granulosa cells cultured in serum- and gonadotropin-free medium secreted progressively less progesterone as time elapsed. Addition of purified high density lipoproteins (HDL) as well as low density lipoproteins [very low density (VLDL) plus low density lipoproteins (LDL)] restored optimal synthesis of progesterone, and HDL was as effective as VLDL + LDL. The use of cholesterol doubly labeled lipoproteins allowed calculation of the proportions of free and esterified cholesterol converted into progesterone. Granulosa cells used either free or esterified cholesterol from VLDL + LDL. In contrast, HDL-esterified cholesterol was a poor substrate for progesterone synthesis, while HDL-free cholesterol was used preferentially. LH increased the use of both kinds of lipoproteins without changing the way in which they were used. Pretreatment of HDL by purified phospholipase A2 increased the conversion of free cholesterol into progesterone. Similar treatment of VLDL + LDL had little effect on progesterone secretion. We conclude that HDL as well as VLDL + LDL can provide cholesterol to human preovulatory granulosa cells and that utilization of HDL-cholesterol may depend on gonadotropin (LH) and enzymatic (phospholipase) regulation.

Cells, Cultured↗
PubMed1985

Triacylglycerol increase in plasma very low density lipoproteins in cyclophosphamide-treated rabbit: relationship with cholesteryl ester transfer activity.

We have studied the cholesteryl ester transfer between HDL and VLDL in cyclophosphamide-treated rabbits, in order to explain the abnormal cholesteryl ester partition between these two lipoprotein classes. The hypertriglyceridemia caused by treatment with the drug was associated with cholesteryl ester- and triacylglycerol-rich VLDL and with HDL poor in esterified cholesterol but relatively enriched in triacylglycerol. These two lipoprotein classes were characterized by their chemical composition and by gel filtration chromatography. VLDL particles were slightly larger in size, compared with controls. Different transfer combinations were envisaged between these abnormal lipoproteins and control ones. The transfer study involved the plasma fraction of d greater than 1.21 g/ml containing the cholesteryl ester transfer protein (CETP). It appeared that the chemical composition of lipoproteins was responsible for the level of cholesteryl ester transfer between lipoproteins. Actually, when the cholesteryl ester acceptor lipoproteins (VLDL) were enriched in triacylglycerol, the transfer was enhanced. Therefore, the effect of lipolysis on the transfer has also been explored. Lipoprotein lipase seemed to enhance the transfer of cholesteryl ester from HDL to VLDL when these lipoproteins were normal, but an important decline was obtained when triacylglycerol-rich VLDL were lipolyzed. This study defines the relationship between lipoprotein chemical composition and transfer activity of cholesteryl ester from HDL to VLDL.

Animals↗
PubMed1982

Platelet arachidonic acid metabolism in severe cerebrovascular disease.

The ability of platelets to synthetise thromboxane B2 and hydroxylated fatty acids from arachidonic acid was studied simultaneously with arachidonic acid-induced aggregation in 42 patients suffering from severe cerebral atherosclerosis and also in 34 healthy controls. Additionally, phospholipase-A2-induced aggregation was performed as a probe for arachidonic acid located at the platelet surface. All the assays were performed with washed platelets, eliminating a possible influence of plasma. Platelets from patients were found responsive to significantly lower concentrations of arachidonic acid whereas thromboxane and hydroxylated fatty acid biosynthesis did not differ from controls. In the experimental conditions used, 75% of the control platelets underwent aggregation with phospholipase A2 plus sphingomyelinase C, in comparison to only 50% for the patients, indicating the necessity for further analysis of the platelet membrane lipids in atherosclerosis.

Adult↗
PubMed1982

Organization and role of platelet membrane phospholipids as studied with phospholipases A2 from various venoms and phospholipases C from bacterial origin.

Phospholipases A2 from various snake or bee venoms and phospholipases C secreted as exotoxins by several bacteria have been used to study the transverse distribution of phospholipids in the platelet plasma membrane and their role in platelet activation. An asymmetric distribution was described for phospholipids, characterized by a preferential localization of sphingomyelin and phosphatidylcholine in plasma membrane outer leaflet, whereas the inner half contains almost all of the anionic procoagulant phosphatidylserine and phosphatidylinositol. Such a distribution might explain the latency of procoagulant activity in resting platelets and implies an intracellular localization of arachidonic acid, the precursor of prostaglandins and thromboxanes. The external arachidonic acid is involved in phospholipase A2-induced aggregation, whereas phospholipase C from Clostridium welchii stimulates platelets through a thromboxane-independent pathway. The latter one is directly linked to the formation of phosphatidic and lysophosphatidic acids, which are able to activate cells through calcium mobilization. So, phospholipase C represents an interesting tool for studying the biochemical processes accompanying stimulation, since it is shown that it mimics the effects of an intracellular phospholipase C, the role of which in platelet activation is discussed.

Animals↗
PubMed1981

Studies on topological distribution of arachidonic acid replacement in platelet phospholipids and on enzymes involved in the phospholipid effect accompanying platelet activation.

In this short review recent results obtained on platelet phospholipid metabolism are summarized. The first part reports a topological study of arachidonic acid (AA) replacement in platelet phospholipids. It is shown that incubation of platelets with radioactive free arachidonic acid leads to a labelling of the phospholipids present inside the platelet, whereas the exchange of intact phosphatidylcholine (PC) molecules with the plasma lipoproteins occurs on the platelet outer surface. This should allow a selective labelling of the small external pool of AA in order to follow its behaviour during platelet activation. In the second part, some enzymes involved in the metabolism of phosphatidylinositol (PI) have been further characterized. The first one is a diglyceride-lipase, which is located in the plasma membrane and releases the two fatty acids esterifying the diglycerides formed from PI by the action of the platelet phospholipase C. Such an enzyme is probably responsible for the release of AA from PI occurring upon platelet activation. On the other hand, cytosolic phospholipid exchange proteins able to catalyse the transfer of PI between membranes have been identified. The possible role of the enzymes involved in the acceleration of PI turnover occurring during platelet activation is discussed.

Arachidonic Acid↗
PubMed1979

Asymmetric distribution of arachidonic acid in the plasma membrane of human platelets. A determination using purified phospholipases and a rapid method for membrane isolation.

1. Non-lytic degradation of human platelet phospholipids have been performed using a combination of bee venom phospholipase A2 (phosphatide 2-acyl-hydrolase, EC 3.1.1.4) and Staphylococcus aureus sphingomyelinase C (sphingomyelin choline phosphohydrolase). Under these conditions, 25.4% of total phospholipds are degraded and 6.4% of total platelet arachidonic acid is released. 2. A new method for rapid isolation of platelet plasma membrane is described, based on the use of [3H]concanavalin A as a membrane marker and of self-generating gradients of Percoll. Plasma membranes are enriched 5.2 fold in lectin marker and 0.43 in N-acetyl-beta-D-glucosaminidase, the main contaminant. This method allows to estimate that 57% of the total cell phospholipids and 61% of the total arachidonic acid content are located in the plasma membrane. 3. The distribution of phospholipids and arachidonic acid between the two leaflets of the plasma membrane has been deduced by using these values and those obtained from non-lytic treatment of intact platelets by phospholipases. It is concluded that 45% of plasma membrane phospholipids, comprising 93% of sphingomyelin, 45% of phosphatidylcholine, 9% of phosphatidylserine, 16% of phosphatidylinositol and 20% of phosphatidylethanolamine form the outer half of the human platelet plasma membrane. The phospholipids appear to bear only 10% of the total membrane arachidonic acid.

Arachidonic Acids↗
PubMed1979

[Familial nonendemic hemolytic uremic syndrome: nephrectomy and transplantation (author's transl)].

A case of familial hemolytic uremic syndrome (HUS) in a four"year-old boy is reported. In his family four adult members are affected with the same disease. In the present patient we decided to perform bilateral nephrectomy because of the inexorable evolution of the disease. The intervention was followed by a distinct improvement, both from the clinical and the laboratory point of view. The child has profited of a renal transplantation. Unfortunately, he died three weeks later because of a severe urological complication. The aim of this study was to examine the effect of bilateral nephrectomy and transplantation on the clinical, laboratory and pathologic anatomical findings, and to analyze the literature, in order to find out whether these measures should be applied in the treatment of familial HUS with severe evolution. The observations seem to confirm the hypothesis of a renal pathogenesis of primary non endemic familial HUS. Nephrectomy seems to stop the disease, and the risk of a recurrence of the HUS after transplantation may be small. The occurrence of the disease in five family members in three generations was interpreted in favour of a genetic predisposition with a dominant gene.

Child, Preschool↗