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C Fressinaud

Publications and source records attributed to C Fressinaud.

At least 37 records · Page 2Linked to original sources
PubMed1990

Normal composition of the major lipids and the distribution of their fatty acids in central nervous system myelin further discriminate mld from shiverer mice.

The primary defect in myelin deficiency (mld), an autosomal recessive mutation in mice with severe hypomyelination of the central nervous system (CNS), is a reduction in the synthesis of myelin basic protein (MBP) due to reduced amounts of MBP-specific mRNA. The present study was performed to determine whether alterations of myelin lipid composition might be associated with this defect. Although a 20-fold reduction of myelin was found in mld brain, the lipid/protein and the phospholipid/sulfatide ratios of purified myelin were unchanged. The analysis of polar lipids demonstrated no striking difference. However, phosphatidylethanolamine (including plasmalogens of the ethanolamine type) was decreased by 7.7% in mld. Fatty acids of total and polar lipids (phospholipids + glycolipids) exhibited a slight decrease in 20:1(n-11) and 20:1(n-9). In conclusion, these results further differentiate mld from its allele shiverer, which shares with mld a dramatic reduction of MBP and absence of major dense line but, in contrast, presents other important biochemical differences in CNS myelin.

Animals↗
PubMed1990

Comparison of the mechanisms of action of insulin and triiodothyronine on the synthesis of cerebroside sulfotransferase in cultures of cells dissociated from brains of embryonic mice.

The effect of low (physiological) concentrations of insulin (2 and 20 ng/ml) and L-triiodothyronine (T3) were studied on two myelin-related enzymes: (1) the 3'-phosphoadenosine-5'-phosphosulfate:cerebroside sulfotransferase (CST, EC 2.8.2.11) catalyzing the production of sulfatide, and (2) the myelin enzyme, 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNP, EC 3.1.4.3.7) in myelinogenic cultures of cells dissociated from embryonic mouse brain. Insulin treatment (20 ng/ml) of the cells in the presence of serum increased CST activity at 18 and 25 days in vitro (DIV) by 86 and 211%, respectively. At 18 DIV and under the same conditions, CNP was significantly stimulated (95%) by high doses of insulin (2,000 ng/ml) only, while arylsulfatase A (EC 3.1.6.1) or cerebroside sulfatase activities, both of which are involved in sulfatide degradation, were unchanged. Thus, it can be assumed that the observed increase of the incorporation of [35S]O4 into sulfatide after insulin treatment of mixed cell cultures is the result of CST induction rather than a decreased catabolism. The level of CST activity in insulin-treated cells (20 ng/ml) in serum-free medium was also increased at 18 and 25 DIV by about 50 and 70%, respectively. Conversely, none of the insulin concentrations used in the absence of serum (even at high doses) had any effect, either at 18 or 25 DIV on CNP and ASA activities. The involvement of insulin in the regulation of sulfatide synthesis was further confirmed by dose-response curves relating the activity of CST to hormone concentration in the medium. The increase in the activity of CST in insulin-treated cells was due only to the increase in the Vmax of this enzyme, suggesting that it may be attributed to enzyme induction. A study of kinetic parameters of CST indicated that there were no differences in pH optimum and Km values between control and induced enzyme. Further experiments using cycloheximide point to a direct effect of insulin on oligodendrocyte CST induction. Data similar to those described above for insulin were also obtained with T3. As for insulin, T3 stimulated the induction of CST but in serum-free medium only. This effect was prevented by cycloheximide. In addition, the induction of CST by T3 was blocked by actinomycin D. This was not the case for insulin. These results suggest that T3 and insulin act on CST by different mechanisms, i.e. at transcriptional and post-translational levels, respectively. Apart from this, the insulin effect on CST activity was additive to that of T3.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

[Partial purification of galactocerebroside sulfotransferase in the rat brain].

We describe a method of partial purification of rat brain 3'-phosphoadenosine-5'-phosphosulfate galactocerebroside sulfotransferase (EC 2.8.2.11, CST). The first steps consist of a Triton X-100 extraction of the enzyme from delipidated microsomes and the fractionation of this extract by precipitation with ammonium sulfate, followed by successive chromatography on hydrophobic gel (phenyl sepharose), heparin, gel filtration (Trisacryl GF2000), hydroxy-apatite and cation exchange resin (SP trisacryl). The denaturation of the enzyme and its instability account for the low enrichment achieved in terms of specific activity, but an evident simplification of the electrophoretic pattern was obtained.

Animals↗
PubMed1989

Regulation of cerebroside sulfotransferase activity in cultured oligodendrocytes: effect of growth factors and insulin.

Cerebroside sulfotransferase (EC 2.8.2.11, CST) specific activity has been determined in oligodendrocyte (OL)-enriched glial cell cultures from newborn rat brain grown in serum supplemented medium. This activity is detectable at 5 days in vitro (DIV) and reaches its maximum value at 12 DIV. This period corresponds to that of oligodendrocyte precursor proliferation in these cultures. The activity decreases thereafter and remains nearly constant after 24 DIV. The developmental curve of CST activity is parallel in pure oligodendrocyte subcultures but twice higher than in primary cultures. These data confirm that CST is highly enriched in OL. Basic fibroblast growth factor (bFGF) (15 ng/ml) and platelet derived growth factor (PDGF) (0.75 U/ml) both enhance CST activity by 90% and 72%, respectively. This increase is in the same range than that of DNA content in treated cultures, whereas protein increase is smaller (50% and 22%, respectively). In contrast, transforming growth factor beta 1 (TGF beta 1, 0.5 and 5 ng/ml) does not significantly enhance CST activity nor DNA content of OL cultures. Insulin at high concentrations (5 micrograms/ml) also enhances CST activity but has no effect at physiological concentrations (20 ng/ml). These results show that CST activity can be controlled by growth factors. They suggest that CST activity is more closely related to OL and OL precursor proliferation than to myelination itself since its maximal activity preceeds myelination in vitro.

Animals↗
PubMed1988

[Autoimmune hypoglycemia: the fault of pyritinol?].

Initially reported in Japan, autoimmune hypoglycemia is related to the presence of insulin-binding antibodies, even in patients who have never been treated with insulin. The authors report a case of spontaneous autoimmune hypoglycemia in a French woman receiving pyritinol. The difference between insulin and C peptide radioimmunoassay levels prompted a search for insulin antibodies. In vitro studies confirmed their presence and showed that they were immunoglobulins G with two binding sites without species specificity. The outcome of autoimmune hypoglycemia is usually favourable, with a rapid decrease of insulin antibodies but steroid therapy is needed when serious clinical manifestations are present. The differential diagnosis with factitious hypoglycemia may be difficult. The reasons for the appearance of the insulin antibodies and the exact mechanisms of hypoglycemia remain hypothetical. However, drugs with a sulfhydril group, such as pyritinol, could play a causative role in this syndrome.

Aged↗
PubMed1988

Cerebellar soluble lectin is responsible for cell adhesion and participates in myelin compaction in cultured rat oligodendrocytes.

Cultures of rat oligodendrocytes were used to test the possible role of the cerebellar soluble lectin (CSL) in myelin formation. Immunocytochemistry at the ultrastructural level showed that the lectin is present in the cytoplasm of the perikaryon of cultured oligodendrocytes and also on the plasma membrane of the cell body and processes. It is present in compact myelin and in the zones of contacts between different myelin sheaths or oligodendrocyte membranes. Staining of blots of the cultures with iodinated CSL indicated that endogenous glycoprotein ligands for CSL are present in the culture, rendering probable the hypothesis that cell contacts between different oligodendrocytes or between adjacent lamellae in myelin are mediated by lectin-glycoprotein interactions. This hypothesis was demonstrated by two effects of anti-CSL Fab fragments (4 micrograms/ml) on oligodendrocyte cultures: (1) the almost complete detachment of the cell layer from the culture substratum, and (2) the loss of myelin compaction by a separation of lamellae at the intraperiod line. The present findings could explain the complexity of the contacts between cultured oligodendrocyte processes by the formation of CSL bridges between glycoproteins of the membranes of these cells. CSL seems to be a key molecule in adhesion both for intercellular contacts and fixation of cells to the substratum. The small number of glycoprotein subunits found in oligodendrocytes that interact with CSL suggests that CSL-mediated cell adhesion involves a special class of glycoprotein glycans.

Animals↗
PubMed1987

Analysis of unsaturated fatty acids of endoneurium and perineurium from normal and degenerating rat sciatic nerve. Morphological correlations.

The major portion of the endoneurial lipids is found in myelin. Since perineurial cells differ morphologically from endoneurial cell components, we attempted to determine whether these morphological differences also extended to a difference in fatty acid (FA) composition. Under normal circumstances, unsaturated FAs are more abundant than saturated ones (55-60% of total FAs) in endoneurium and perineurium. A characteristic biochemical difference between these two structures lies in the distribution of linoleic acid (C18:2(n-6)) which represents 20% of total FAs in perineurium and only 2% in endoneurium. Wallerian degeneration takes place after injection of pure glycerol into the endoneurium. This is followed by regeneration characterized by a proliferation of perineurial cells infiltrating the center of the nerve fascicule forming microcompartments. The changes in linoleic acid content reflect these morphological changes. A marked increase in linoleic acid is detected in the endoneurial fraction in parallel with the observed infiltration of perineurial cells into the nerve fascicule.

Animals↗
PubMed1987

Changes in composition of endoneurial and perineurial fatty acids during glycerol-induced Wallerian degeneration and regeneration in the sciatic nerve of the adult rat.

Intraneural injection of pure glycerol induces Wallerian degeneration with subsequent regeneration. In agreement with other reports, we observed an increase in endoneurial polyunsaturated fatty acids 8 days after the glycerol injection. Levels then fell until day 30. After a period of 5 months, there was an increase in C18:2(n-6) in the intrafascicular tissue, concomitant with a marked fall in this fatty acid in the remaining extrafascicular perineurium. The rise in C18:2(n-6) in endoneurium correlated with infiltration of this tissue by perineurial cells. Interactions between perineurium and endoneurium during nerve regeneration are discussed.

Animals↗
PubMed1986

Fatty acid composition of endoneurium and perineurium from adult rat sciatic nerve.

Reports on lipid composition of peripheral nervous system have generally been restricted to the saturated fatty acids of the endoneurium. In this work we attempt to determine the fatty acid composition of the different lipid classes in both endo- and perineurium from sciatic nerve microdissection on adult rats. Unsaturated fatty acids were found to make up around 60% of total fatty acids in samples of endoneurium and perineurium, with monounsaturated fatty acids forming 40-50% of total unsaturated fatty acid content. Although the same fatty acids were present in both tissues there was a striking difference in C 18:1 (n-9) and C 18:2 (n-6) ratio between endoneurium and perineurium, which is particularly rich in linoleic acid. The nonpolar perineurial lipids were found to be richest in linoleic acid. Phospholipids were present in the perineurium, and they contained high proportions of saturated and medium-chain monounsaturated fatty acids.

Animals↗
PubMed1986

Acute pure sensory paraneoplastic neuropathy with perivascular endoneurial inflammation: ultrastructural study of capillary walls.

We studied a patient with epidermoid carcinoma of the lung (treated surgically 1 year earlier) and an acute symmetric pure sensory neuropathy that regressed almost completely within 1 month. Superficial peroneal nerve biopsy 15 days after onset showed evidence of demyelination with perivascular endoneurial inflammation. On ultrastructural examination, lymphocytes were seen passing through endothelial cells of endoneurial capillaries.

Capillaries↗
PubMedDate not supplied

[Multiple sclerosis: review of main experimental data and pathogenic hypotheses].

The pathogenesis of multiple sclerosis (MS) is considered from three different viewpoints: genetic, viral and immunological. A genetic predisposition intervenes, as testified by the familial forms of MS and by the frequency of HLA A3B7 and DR2 groups in MS patients. The hypothesis of an inherited enzyme deficiency in oligodendrocytes is discussed. Many viruses are known to induce demyelination in animals, and the intrathecal production of antibodies to measles virus as well as the in vitro discovery of DNA transcripts of this virus in patients are suggestive of a viral factor. Experimental allergic encephalomyelitis (EAE) and chronic EAE have made it possible to study the immune and other mechanisms which might be involved in MS. While the myelin basic protein and the M2 antigen appear to be the first antigen targets, the demyelinating agents in this model are antibodies to galactocerebroside. The factors responsible for demyelination in MS have not yet been elucidated, but the antibodies present in the cerebrospinal fluid do not seem to be demyelinating in vitro. Descriptions of the cells which constitute the lesions and of the antigen markers they express suggest that endothelial cells and astrocytes (possibly presenting antigens to lymphocytes) might play a part in the genesis of the lesions. Experiments concerning the modulation and suppression of EAE allow new therapeutic approaches to be envisaged.

Animals↗
PubMedDate not supplied

[Developmental adrenal tuberculosis. Value of x-ray computed tomography].

Two cases of Addison's disease secondary to active adrenal tuberculosis are reported. Computed tomography showed hypertrophy of the adrenal gland, which was bilateral in one case and unilateral in the other. Repeat computed tomography scans during antituberculous chemotherapy demonstrated a progressive change of the adrenals toward atrophy and calcification, while the adrenal function remained impaired. The authors recall that adrenal tuberculosis may be unilateral first, then bilateral, and that the gland is initially hypertrophic before hormonal deficiency appears; later on, adrenal atrophy and calcification develop. Computed tomography seems to be useful in the aetiological diagnosis of Addison's disease. Moreover, it helps in determining whether or not antituberculous therapy is indicated, which is not always easy to decide in the absence of "active" focus. The finding, with or without positive tuberculin skin tests, of an adrenal hypertrophy unexplainable by any other pathology (e.g. metastasis, histoplasmosis) should call for antituberculous treatment, especially since it sometimes results in recovery of adrenal function.

Addison Disease↗