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S Marie

Publications and source records attributed to S Marie.

27 records · Page 2Linked to original sources
PubMed1993

The pyruvate kinase gene as a model for studies of glucose-dependent regulation of gene expression in the endocrine pancreatic beta-cell type.

The insulinoma beta-cell line INS-1 expresses the L-type pyruvate kinase gene at high level and responds to a rise in extracellular glucose by strong induction of gene expression. Following the addition of glucose to the culture medium in the 3.5-33 mM concentration range, the cellular level of L-type pyruvate kinase mRNA increases within 2 h and reaches a maximum 15-fold above basal in 8-12 h. By run-on nuclear assay, the relative transcription rate of the pyruvate kinase gene is shown to increase 4-fold at maximal stimulation, suggesting that both transcriptional and post-transcriptional effects contribute to mRNA accumulation. The glucose effect is totally suppressed by the hexokinase inhibitor mannoheptulose, indicating a requirement for glucose phosphorylation. The mRNA induction is not inhibited in glutamine-free culture medium or by azaserine, suggesting that the hexosamine biosynthetic pathway is not involved. Moreover, metabolism along the glycolytic pathway does not appear to be an absolute requisite, since 2-deoxyglucose partly mimics the inductive effect of glucose. The glucose effect on the pyruvate kinase gene is reversibly antagonized by agents increasing intracellular cAMP. In addition, the effect is highly specific to the pyruvate kinase gene. Neither proinsulin I mRNA nor glucokinase mRNA are increased in glucose-stimulated INS-1 cells. Short term transfection with CAT plasmids driven by the pyruvate kinase L promoter reveals specific glucose-inducible reporter activity with the 183-base pair promoter region upstream of the cap site. Within this region, the previously described L4 cis-acting element is crucial for glucose responsiveness, as demonstrated by the fact that a plasmid with a mutation in this element does not elicit glucose-inducible CAT activity. Induction of L-type pyruvate kinase mRNA occurs in the islets of rats subjected to fasting and carbohydrate refeeding. In conclusion, the L-type pyruvate kinase gene provides an interesting model of glucose-regulated gene in the endocrine beta-cell type.

Animals↗
PubMed1993

Age- and tissue-dependent expression of CYP2C23 in the rat.

A cDNA was isolated from a library prepared with 15-day-old rat liver RNA and was shown to correspond to CYP2C23 with some minor alterations which modified the open reading frame. The expression of CYP2C23 was examined in rat liver, kidney, lung and testis and during ontogenesis. An appreciable amount of CYP2C23 RNA was observed in liver and kidney but the age-dependent expression was quite different between these two tissues. In liver, expression reached its maximal value in early neonates and remained quite stable, while the increase was progressive in kidney before declining after 3 weeks of age. In the liver, classical inducers of cytochrome P-450 decreased the CYP2C23 RNA content. Experimental data confirm the classification of CYP2C23 as a constitutive member of the 2C subfamily and clearly establish its age- and tissue-dependent expression in rat.

Aging↗
PubMed1993

[Musical hallucinations: 7 cases].

Musical hallucinations (MH) occurred in 7 patients (5 women and 2 men, age 58-90 yrs) with mild to severe unilateral or bilateral deafness. The hallucinations usually consisted of musical memories (childhood songs, past "hits"). They started abruptly and were identified, sometimes after a period of doubt, as hallucinations. They became "louder" in the silence and, when iterative, could be distressing. By concentrating, 3 patients could change the ongoing tune for another. Elementary (1 case) or verbal (3 cases) auditory hallucinations could be associated and, in one case, vivid visual hallucinations occurred which were not criticized. One patient suffered depression and the MH faded after antidepressive treatment. In the other cases, no psychiatric disorder was identified. Neurological examination, EEGs and brain MRI (in 5 cases) were normal in all but one case, in which MH followed seizures secondary to a left parietal metastasis. Such MH may be termed hallucinosis according to Ey's description. They share some characteristics with other hallucinatory phenomena associated with sensory deprivation, such as the Charles Bonnet syndrome and "pain memories" in phantom limbs. However, the role of deafness, the underlying central mechanisms and psychological factors are poorly understood.

Aged↗
PubMed1989

Phenobarbital-inducible gene expression in developing rat liver: relationship to hepatocyte function.

The expression of phenobarbital-, pregnenolone 16 alpha-carbonitrile- and polycyclic aromatic hydrocarbon-inducible cytochromes P-450 and of phenobarbital-inducible UDP-glucuronosyltransferase was examined in developing rat liver. RNAs coding for these proteins were present in fetal rat liver and their respective concentrations remained quite stable in non-induced animals. Inducers differently affected the concentration of RNAs: clofibrate had no action, whereas methylcholanthrene was highly active in fetal liver. Induction by phenobarbital gradually increased during ontogenesis, in parallel with the augmentation of the number of hepatocyte cells in the liver. Our contribution definitively demonstrates that the ability of phenobarbital to enhance P-450 and UDPGT RNAs is strictly restricted to hepatocytes and remains roughly unchanged throughout ontogenesis. In addition, phenobarbital was also able to potentiate the inducing capacity of methylcholanthrene (i.e., raising the TCDD-binding protein) exclusively in hepatocytes. This is the first direct evidence that the number of hepatocytes in the liver, rather than a biochemical maturation, controls the expression of phenobarbital-inducible genes. Pregnenolone 16 alpha-carbonitrile was also effective as inducer in fetal and neonatal rats and its maximal effect was observed in 5-d-old neonates, suggesting a regulation mechanism temporally different from that of phenobarbital.

Animals↗
PubMed1989

Ontogeny and regulation of drug metabolism in humans. Phase I: Monooxygenases.

Most data concerning the development and regulation of cytochrome P-450-dependent monooxygenases were obtained in experimental animals, especially rats, by two successive approaches: first, the assay of total liver cytochrome P-450 and of related monooxygenase activities; then, more recently, the immunoquantification of molecular forms of cytochrome P-450, and the estimation of corresponding mRNAs with nucleic acid probes. Results were compared, before and after birth, in untreated animals, and in animals treated by inducers, mainly phenobarbital and polycyclic aromatic hydrocarbons. For evident ethical reasons, fewer data could be obtained in human liver during development. However, the availability of specific antibodies and nucleic acid probes recently allowed some progress in the comparison of the isoenzyme pattern of cytochromes P-450 in fetal and adult human liver.

Aging↗
PubMed1988

Expression of cytochrome P-450 isozymes in the liver of hypophysectomized rats. Evidence for different regulation mechanisms concerning P450IIB and P450IIIA subfamilies.

1. Monooxygenase activities have been examined in rat liver to determine the effects of castration and hypophysectomy on cytochrome P-450 species. In adult males, hypophysectomy caused a decrease of total P-450 concentration, aniline hydroxylase, benzopyrene hydroxylase, benzphetamine demethylase, testosterone hydroxylase and imipramine hydroxylase and demethylase activities. The treatment of hypophysectomized animals with human growth hormone or testosterone did not restore the full activity. 2. When probed with antibodies, microsomes from hypophysectomized males and females exhibited an intense reaction with a polyclonal anti-(phenobarbital-induced P-450) which was not observed with a monoclonal antibody of anti-(phenobarbital-induced P-450). 3. These microsomal preparations also reacted with an antibody raised against a developmentally regulated P-450. No sex difference could be detected with this antibody. Furthermore, administration of human growth hormone to hypophysectomized males prevented this immunoreaction. 4. Total RNA has been prepared from the same liver; when probed with cDNAs, no changes occurred in the content in P-450 b/e, PB 24 (a constitutive member of the phenobarbital subfamily) and phenobarbital-inducible mRNA for UDP-glucuronosyltransferase. 5. In contrast, P-450 mRNA induced by pregnenolone 16 alpha-carbonitrile was modulated by hormonal manipulations: lower in females and castrated males than in intact males, increased in both sexes after hypophysectomy. Treatment of hypophysectomized males with human growth hormone abolished this rise in pregnenolone-16 alpha-carbonitrile-induced P-450 mRNA accumulation. Data collected in this study support the assumption that hypophysectomy acts differently on the regulation of various P-450 isozymes and that this regulation clearly does not involve the phenobarbital subfamily of P-450s.

Aniline Hydroxylase↗
PubMed1988

Transplacental induction of cytochromes P-450IA1 and P-450IA2 by polycyclic aromatic carcinogens: TCDD-binding protein level as the rate-limiting step.

Induction of cytochromes P-450c and P-450d have been compared in fetal and adult rat liver. A single dose of 3-methylcholanthrene (MC) 16 h before death, resulted in a pronounced accumulation of both mRNAs in adult liver. In contrast, treatment of fetuses with a single dose of MC did not increase the hepatic content in P-450c and P-450d mRNAs, whereas a 3-day treatment gave rise to a considerable accumulation of mRNAs. The fetal rat liver content in 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD)-binding protein was extremely low compared to the adult content. Pretreatment of fetuses with phenobarbital potentiated the inducing effect of MC upon P-450c and P-450d mRNA accumulation in relation to the duration of pretreatment, as well as increasing the hepatic content in TCDD-binding protein. Data strongly suggest that the hepatic TCDD-binding protein level is the rate-limiting step in MC induction of P-450c and P-450d in fetal but not in adult rat liver. In addition, phenobarbital and MC are potent inducers of the TCDD-binding protein in the fetal rat liver.

Animals↗