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Biomedical subjects

C Rougeot

Publications and source records attributed to C Rougeot.

At least 37 records · Page 2Linked to original sources
PubMed1994

GABAA and NMDA receptor activation controls somatostatin messenger RNA expression in primary cultures of hypothalamic neurons.

GABAA receptors mediate the inhibition of somatostatin gene expression and NMDA receptors mediate its stimulation. The aim of this study was to determine whether the two major neurotransmitters in the central nervous system (GABA and glutamate) could interact to control somatostatin mRNA content in primary cultures of hypothalamic neurons. Neurons were incubated for 15 min on days 3, 5, 7 or 11 of culture with Mg(2+)-free medium containing either NMDA (20 microM) or bicuculline (50 microM) to investigate the ontogenesis of somatostatin somatostatin secretion in response to NMDA and GABA. We found that NMDA significantly elicited somatostatin release from day 3, and bicuculline-induced release was observed from day 5. An ontogenetic study of somatostatin mRNA levels revealed that it steadily increased up to day 5 (6-fold) and a slight but nonsignificant decrease was observed on day 7 which stabilized until day 13. Experiments were thus carried out on day 11 of culture. Pharmacological manipulations of the two types of receptors (NMDA and GABAA) were performed to study the effect of the interaction on somatostatin mRNA accumulation. Time-course studies revealed the optimal time of action of the neurotransmitters (20 h). Our results demonstrated that bicuculline-induced mRNA accumulation was not additive with that elicited by NMDA after 20 h of incubation. In contrast, (+)-5-methyl-10,11-dihydro-5H-dibenzo(a,d')cyclohepten-5,10-imine hydrogen (MK-801) at 10 microM completely abolished the stimulatory effect of bucuculline during the same time period. In addition, muscimol was unable to decrease somatostatin mRNA levels when NMDA receptors were blocked by MK-801.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Chronic stress affects in vivo hypothalamic somatostatin release but not in vitro GH responsiveness to somatostatin in rats.

One week after stereotaxical implantation of a push-pull cannula into the median eminence (ME), rats were stressed by immobilization for 2 h daily for 7 days. Thereafter, ME was perfused for 1 h in basal, stress and recovery conditions, respectively, and somatostatin (SRIH) was measured in perfusate fractions. Pituitaries were in vitro perifused to assess GH responsiveness to SRIH. In the stressed group, basal SRIH release was significantly higher than in the control group and stress caused a significant sharp peak in neurohormone release. GH responsiveness to SRIH was not affected in pituitaries obtained from stressed donors. High SRIH levels secreted under chronic stress thus did not impair the GH pituitary response to SRIH.

Animals↗
PubMed1993

GABA inhibition of somatostatin gene expression in cultured hypothalamic neurones.

GABAA receptors mediate the inhibition of somatostatin release in hypothalamic neurones. To study the possible effect of GABA on somatostatin biosynthesis, somatostatin and preprosomatostatin mRNA levels were evaluated after exposure of hypothalamic neurones to muscimol or bicuculline. Muscimol (50 microM) decreased preprosomatostatin mRNA levels, by 25% after 4 h and 30% after 24 h treatment. Bicuculline (50 microM and 100 microM) increased preprosomatostatin mRNA levels by 1.4 and 1.5 fold after 4 h and by 1.3 and 1.7 fold after 24 h treatment. Somatostatin content was not modified after muscimol or bicuculline exposure. Total DNA content, used to control cellular viability, was not modified under any experimental conditions. Our findings suggest that the GABAergic inhibition of mRNA levels could be a consequence of the GABA inhibition of somatostatin release, thus allowing limited changes in peptide steady-state levels.

Actins↗
PubMed1993

Localization of mRNAs of two androgen-dependent proteins, SMR1 and SMR2, by in situ hybridization reveals sexual differences in acinar cells of rat submandibular gland.

Androgen-dependent sexual differences in the granular convoluted tubules of mouse and rat submandibular glands (SMG) have been extensively reported. We studied two major androgen-dependent mRNAs of the rat SMG encoding proteins named SMR1 and SMR2. To determine which cell type in the SMG is responsible for synthesis of these mRNAs, we performed in situ hybridization with digoxigenin-labeled RNA probes coupled with alkaline phosphatase detection. We show that SMR1 and SMR2 mRNAs are synthesized in the acinar cells of the SMG. A clear difference in SMR1 and SMR2 mRNA levels in male and female is demonstrated. During the course of this study we also confirmed the acinar localization of mRNAs encoding the glutamine/glutamic acid-rich proteins (GRP) of rat SMG. Our data are the first clear evidence of androgen-dependent sexual differences in acinar cells of rat submandibular gland.

Animals↗
PubMed1991

Effects on metabolic and hormonal parameters of monosodium glutamate (umami taste) ingestion in the rat.

Umami taste appears to signal, at the gustatory level, the intake of proteins, therefore the working hypothesis was: does umami taste of a monosodium glutamate (MSG) solution elicit changes in both glucagon and insulin release, similar to those elicited by amino acids, and consequently, changes in plasma glucose and in overall cellular metabolism? In a first experiment, rats were equipped with indwelling jugular and oral catheter and serial samplings were made in the free moving, undisturbed rat before and after an oral or IV infusion of MSG (0.05 M). None of the plasma parameters showed any significant response. In a second experiment, energy expenditure was monitored by means of an original computer-based calorimeter capable of calculating, besides the classical parameters, resting metabolism in a moving animal (designated by background metabolism). The addition of MSG to a low calorie, low-protein meal did not modify background metabolism or respiratory quotient. Therefore MSG ingestion does not by itself affect plasma levels of hormones of glucose and protein metabolism, total metabolism rate, or nutrient utilization. However, examination of individual data and those from a pilot experiment for future work suggests that MSG becomes an efficient metabolic effector if added to a caloric diet, and so enhances proper thermogenesis of macronutrients.

Animals↗
PubMed1991

Comparative study of biosynthetic human growth hormone immunogenicity in growth hormone deficient children.

The immunogenicities of six recombinant human growth hormone (rhGH) preparations, from KABI (A rhGH191 and B rhGH192), Eli Lilly (C), Nordisk (D), Sanofi (E) and Serono (F), used to treat 260 GH-deficient children, have been compared using a common specific and sensitive procedure for antibody determination. For this purpose we developed two immunoassays: a competitive liquid radioimmunoassay using 125I-rhGH, and an immunometric solid enzymoimmunoassay in which the rhGHs were immobilized. Blood samples were collected from the GH-deficient children before treatment and after 3, 6, 9, 12, 18 and 24 months of therapy. Human GH antibodies were detected in children treated with 3 of the 6 rhGH preparations. Seven percent of the patients treated with hormone A, 14% with hormone B and 22% with hormone C formed antibodies against the respective rhGH. Differences in capacity and affinity of the hGH antibodies were observed between these anti-GH-positive groups. They could be divided into 2 groups according to their immunopotency. One group (7, 14 and 6% of the patients treated with hormones A, B and C, respectively) developed anti-hGH antibodies with very low binding capacities (30-100 fmol/ml). The other group (16% of the patients treated with hormone C) developed IgG-type antibodies to hGH with higher binding capacities (200-1,200 fmol/ml) and a measurable binding affinity (Ka = 10(8) M-1). These hGH antibodies partially inhibited the binding of labeled GH to its specific liver membrane receptor. However, because of their low titer, they did not inhibit growth in the treated children.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Estradiol increases the secretion by MCF7 cells of several lysosomal pro-enzymes.

The synthesis and secretion of pro-cathepsin D is increased by estrogens in MCF7 cells. We quantified the effect of estradiol on other lysosomal enzymes in order to investigate the mechanism of this hypersecretion. Precursors of beta-hexosaminidase, cathepsin B and beta-galactosidase, which are routed to lysosomes via the mannose-6-phosphate (Man-6-P) receptor, were secreted in much lower amounts than pro-cathepsin D, but their secretion was also increased by estradiol. The activity of acid phosphatase, which is routed to lysosomes via a different transmembrane mechanism, was not altered by estradiol. While estradiol stimulated gene expression of pro-cathepsin D, it had no effect on that of pro-cathepsin B. We conclude that estradiol stimulates the secretion of several lysosomal pro-enzymes in MCF7 cells, suggesting that a general mechanism is responsible for this derouting rather than a specific alteration of cathepsin D structure.

Breast Neoplasms↗
PubMed1990

Leukotriene C4-induced release of LHRH into the hypophyseal portal blood and of LH into the peripheral blood.

Intracerebroventricular (i.c.v.) administration of leukotriene (LT) C4 at doses of 2, 0.5 and 0.2 micrograms/rat significantly stimulated (3-12 fold) the release of LH into the peripheral blood of male rats. Injection of anti-LHRH serum had no effect on LTC4-stimulated LH release, but did block PGE2- stimulated LH release. I.c.v.- infused LTC4 also stimulated the release of LHRH into the hypophyseal portal blood. This is the first report of an in vivo action of LTC4 on the release of a hypothalamic releasing factor (LHRH) and a pituitary hormone (LH). These observations, plus in vitro results, clearly show that LTC4 stimulates LH release by acting on both the hypothalamus, causing LHRH release, and on the pituitary. Then the action of LTC4 on LH release in vivo is quite different from the indirect action of PGE2.

Animals↗
PubMed1990

Detection of synenkephalin, the amino-terminal portion of proenkephalin, by antisera directed against its carboxyl terminus.

Synenkephalin (SYN), the nonopioid amino-terminal portion of proenkephalin (PRO), is stable and well conserved in mammals and therefore a promising marker for PRO systems. We immunized rabbits with synthetic [Tyr63]SYN(63-70)-octapeptide, coupled by glutaraldehyde to bovine serum albumin. In radioimmunoassay (RIA) using antiserum no. 681, [Tyr63]SYN(63-70)-octapeptide as standard, and 125I-[Tyr63]SYN(63-70)-octapeptide as tracer, the IC50 was approximately 51 fmol/100-microliters sample at equilibrium or 12 fmol/100 microliters in disequilibrium, and the sensitivity was approximately 3 fmol/100 microliters. Cross-reactivity of the assay was 100% with [Cys63]SYN(63-70)-octapeptide and with bovine adrenal 8.6-kilodalton peptide digested with trypsin and carboxypeptidase B, but less than 0.1% with transforming growth factor-alpha, less than or equal to 2 x 10(-6) with Leu-Leu-Ala [SYN(68-70)-tripeptide], and much less than 10(-6) with all other peptides tested. Therefore in RIA this antiserum is specific for the free carboxyl terminus of SYN. Because the peptide detected after enzyme digestion is the complete SYN(63-70)-octapeptide, we refer to the RIA as an assay for SYN(63-70). Tissue extracts were made in 1 M acetic acid, dried, reconstituted in Tris-CaCl2, and digested sequentially with trypsin plus carboxypeptidase B. Extracts from bovine corpus striatum gave SYN(63-70) RIA dilution curves parallel to the standard curve both before and after digestion. Digestion increased the amount of immunoreactive SYN(63-70) in striatum by a factor of 1.5-2.0. The ratio of total immunoreactive [Met5]enkephalin to total immunoreactive SYN(63-70) (after sequential digestion) was approximately 6:1. At least 90% of the immunoreactive SYN(63-70) in extracts of bovine caudate nucleus eluted from Sephadex G-100 with an apparent molecular weight equal to that of bovine PRO(1-77). Using the new RIA we were able to detect and characterize SYN processing for the first time in extracts of whole rat brain, human globus pallidus, and human pheochromocytoma. Results in these tissues were similar to those in cattle, in that most stored SYN had been processed to a free carboxyl terminus. Since the C-terminal octapeptide of SYN is practically identical in all known mammalian PRO, antiserum no. 681 should be useful for detecting, measuring, and purifying SYN from various mammals, including human beings.

Adrenal Gland Neoplasms↗
PubMed1990

Intracerebroventricular injection of platelet-activating factor induces secretion of adrenocorticotropin, beta-endorphin and corticosterone in conscious rats: a possible link between the immune and nervous systems.

To investigate whether platelet-activating factor (PAF) exerts an indirect action on immune cells by altering the secretion of hypothalamic-pituitary-adrenal (HPA) axis products, the effects of intracerebroventricular (i.c.v.) PAF on adrenocorticotropic hormone (ACTH), beta-endorphin and corticosterone blood levels were examined in adult male rats. Hormones were radioimmunoassayed on blood samples from conscious or ether-anesthetized rats after i.c.v. injection of PAF or vehicle into the left lateral ventricle. PAF induced significant increases in these stress-related hormones under both, basal and ether-induced stress conditions. The analysis of the time course response to PAF of hormone release into the blood of unrestrained rats revealed that: i.c.v. injection of 5.4 nmol PAF resulted in rapid increases in ACTH and beta-endorphin, at the latest within 15 min after the onset of injection. The maximal response of both hormones was reached within 45 min after the onset of injection and was followed by an elevation of plasma corticosterone. Hormone release is related to the PAF dose infused, the lowest effective PAF concentration was 1 nmol. The stimulatory effect of PAF on ACTH and beta-endorphin secretion was strongly decreased in rats previously treated with purified anti-rat corticotropin-releasing factor (CRF) antibody. These results, associated with the in vitro demonstration that PAF increases CRF release from incubated rat median eminence, strongly support the hypothesis that the stimulatory action of PAF on the secretion of HPA axis products is mediated at least partly, by stimulating hypothalamic CRF release.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1990

[Early prediction of risk of bronchopulmonary dysplasia].

Bronchopulmonary dysplasia (BPD) has become a frequent and worrying issue in neonatal intensive care units (NICU). The aim of this retrospective study was to define more precisely the incidence of BPD within a population of 2,216 newborns admitted at less than 24 hrs of life. 138 cases of BPD were diagnosed. The BPD rates decrease exponentially with regard to gestational ages (GA) [67% at less than 28 weeks (w), 37% at 28-29 w, 22% at 30 w, 9% at 31-32 w, 3% at 33-34 w and 0.4% at greater than or equal to 35 w]. The presence of hyaline membrane disease (HMD) increases the GA related risks by 1.5, 2, 3, 10, 20 and 40 times at less than 28 w, 28-29 w, 30 w, 31-32 w, 33-34 w and greater than or equal to 35 w, respectively. Other factors such as interstitial emphysema, refractory hypoxemia and hypotrophy associated with HMD, have been found associated with increased risks. A chart taking into account all these parameters has been constructed allowing the determination of individual risks of developing BPD during the first days of life.

Bronchopulmonary Dysplasia↗
PubMed1990

[Evaluation of short term prognosis of bronchopulmonary dysplasia].

Assessing the short-term prognosis of bronchopulmonary dysplasia (BPD) (duration of mechanical ventilation, of O2 therapy, and risk of death) is often uncertain at the early stages of the disease. From a retrospective study of 124 cases of BPD, we made a search for factors of poor prognosis which could be recognized early. Among the 124 BPD, 56 (45%) had a severe disease (mechanical ventilation for greater than 3 months and/or O2 for greater than 4 months), and 24 of them (20%) died. Two types of factors have been identified as linked to a poor prognosis (risk of evolution towards a severe disease in a proportion of 70 to 90%): some respiratory events (refractory hypoxemia, recurrent pneumothorax, interstitial emphysema, no improvement of hyaline membrane disease at 3-4 days of life in babies less than 32 weeks gestational age) and hemodynamic failures (cardiac failure due to persistent ductus arteriosus, collapse following infection or anoxia). We have also defined different values of a ventilatory index (I = mean airway pressure x FiO2) which allows the neonatologists to estimate the final prognosis of BPD during the first two months of life.

Airway Resistance↗
PubMed1990

[Pre-eclampsia: a cause of fetal heart failure?].

The authors report the case of a newborn whose mother presented with pre-eclampsia. Intrauterine growth retardation, peripheral edema, ascitis and pleural effusion were present at birth. The authors suggest that placental vascular abnormalities could be responsible for fetal heart failure and edema syndrome.

Adult↗
PubMed1989

Adrenocortical response following acute neurogenic stimuli is mediated by CRF-41.

The present study examined whether neurogenic stimuli activate the pituitary-adrenal axis via CRF-41. Adult male rats were exposed to photic, acoustic or sciatic nerve stimulation. At 4, 15, and 30 min following the onset of stress, animals were sacrificed, trunk blood collected and the median eminence removed. At 4 min following the stress onset, there was a significant decrease in CRF-41 content of the median eminence, which persisted for 30 min. Concomitant with the decrease in CRF-41 content, serum adrenocorticotropic hormone (ACTH) and corticosterone levels increased. Thus, this study demonstrates that CRF-41 released from the median eminence plays a dynamic role in mediating the ACTH and corticosterone response to neurogenic stimuli.

Adrenal Cortex↗
PubMed1989

Increased secretion, altered processing, and glycosylation of pro-cathepsin D in human mammary cancer cells.

In human mammary cancer cells, pro-cathepsin D (pro-Cath-D) is induced by estrogens and 50% of it is secreted. To determine whether its secretion is characteristic of mammary cells or transformed cells, we compared its production, processing, and glycosylation in primary cultures of normal mammary epithelial cells to those found in breast cancer cell lines. The cytosolic concentration of total cathepsin D (precursor and mature enzyme) measured by enzyme-linked immunosorbent assay was 8 times higher in cancer cells. Its mRNA level estimated by Northern blot analysis was 8 to 50 times higher and its secretion was 30 times higher in cancer cells. Using pulse-chase labeling, the cellular processing of pro-Cath-D was altered in hormone-dependent and -independent breast cancer cells in comparison to normal cells. This alteration resulted in a lower accumulation of mature enzyme, while the secretion and cytoplasmic accumulation of pro-Cath-D was greater in breast cancer cells than in normal cells. NH4Cl increased secretion of the proenzyme in normal cells but not in cancer cells. The secreted proenzyme was markedly heterogeneous and had a more acidic pI in MCF7 cells than in normal mammary cells. These acidic forms disappeared following endo-beta-N-acetylglucosaminidase H treatment indicating that the structural difference between pro-Cath-D of normal and of cancer mammary cells was located on high mannose or hybrid N-linked oligosaccharides. This difference may be responsible for the altered routing of the pro-Cath-D in breast cancer cells.

Breast↗