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Biomedical subjects

C Jacquemin

Publications and source records attributed to C Jacquemin.

At least 55 records · Page 3Linked to original sources
PubMed1989

Activation of S6 kinase in astroglial cells by FGFa and FGFb.

Basic (b) and acidic (a) forms of the fibroblast growth factor (FGF) promoted a rapid increase of the cytosolic S6 kinase activity in astroglial cells. S6 kinase activity was maximal 10 min after addition of the factors to cell cultures and remained at this level for at least 30 min. Half-activation of the enzyme was obtained with 3 ng/ml FGFa. Heparin (100 micrograms/ml) potentiated the response to suboptimal concentrations of FGFa. This growth factor appeared to stimulate an astroglial S6 kinase resembling that stimulated by insulin, IGF1, TPA and cAMP. Although FGFb is more potent than FGFa in stimulating proliferation of Chinese hamster lung fibroblasts (CCL39), it was not more efficient than FGFa in stimulating the S6 kinase activity of astroglial cells.

Animals↗
PubMed1989

Induction of type II 5'-deiodinase activity in cultured rat astroglial cells by 12-O-tetradecanoylphorbol-13-acetate: dependence on glucocorticoids.

The effect of an activator of protein kinase C, 12-O-tetradecanoylphorbol-13-acetate (TPA), on the 5'-deiodinase (5'D) activity was studied in rat astroglial cells cultured in chemically defined medium. TPA promoted a large increase in the type II 5'D activity, which was maximal 5-10 h after addition of TPA and then declined to the basal level at 24 h. The optimal TPA concentration was 10(-7) M. TPA and 8-Br-cAMP, an other inducer of 5'D activity were antagonist. Otherwise, TPA stimulated 5'D activity only in the presence of glucocorticoids at concentrations from 10(-8) M to 10(-4) M. Glucocorticoids alone induced a slight increase in 5'D activity. These data indicate that protein kinase C contributes to the control of 5'D activity in astroglial cells and that its action is dependent on glucocorticoids.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1989

[Iatrogenic femoral pseudo-aneurysm. Analysis of the causes, diagnosis and treatment. Study of 12,248 arterial catheterizations].

Pseudoaneurysm is a classical but unusual complication of femoral catheterism. 22 cases are reviewed: 19 occurred after coronarography, 2 after peripheral percutaneous angioplasty and only one after a renal diagnostic arteriography. In all cases, the diagnosis of the pseudoaneurysm was established by I.V. D.S.A. 2 different medical teams are distinguished: the first using small catheters (4 and 5 F), the second using larger catheters (7 and 8 F) which are more aggressive. Two factors allow to avoid this complication: the diameter of the catheter and a correct compression dressing. The treatment of this complication, usually surgical, consisted in a simple manual percutaneous compression in 3 patients.

Aneurysm↗
PubMed1989

[A model for studying the transmission of information produced by certain growth factors: activation mechanisms of S6 kinase in cultured astrocytes].

Treatment of cultured astrocytes from 2-day-old rat cerebral hemispheres with insulin, somatomedin C (IGF1), thrombin and acidic or basic fibroblast growth factors promoted a rapid activation of a cytosolic protein kinase (S6 kinase) which phosphorylates ribosomal protein S6. The phorbol ester (TPA) also triggered a rapid increase in S6 kinase activity. Two agonists of adenylate cyclase activity (forskolin and isoproterenol) and the cyclic AMP analog (dibutyryl cAMP) also stimulated the same S6 kinase. These observations support the idea that several pathways might promote the activation of the same entity that is regarded as one of the primary targets of signals elicited by growth factors.

Animals↗
PubMed1988

Purification and characterization of phospholipase A2 inhibitory proteins from pig thyroid gland.

A 32 kDa phospholipase A2 inhibitory protein was isolated from pig thyroid gland after calcium precipitation and fast protein liquid anion-exchange chromatography. SDS-polyacrylamide gel electrophoresis revealed the purity of the protein. The protein activity was assessed by the inhibition of pancreatic phospholipase A2 on [3H]oleic acid-labelled Escherichia coli membranes as substrate and on the prostaglandin E2 production of cultured thyroid cells. The amino acid composition and the isoelectric point were quite similar to those of endonexin previously described in other tissues or cells. The cross-reactivity of a polyclonal antibody against a 32 kDa lipocortin from human peripheral blood mononuclear cells with our thyroidal 32 kDa protein confirmed its lipocortin nature. Before the purification by fast protein liquid chromatography, the Ca2+ pellet contained lipocortin I (35 kDa and its core protein 33 kDa) identified by its cross-reactivity with a polyclonal antibody.

Amino Acids↗
PubMed1988

Phorbol ester prevents the thyroid-stimulating-hormone-induced but not the forskolin-induced decrease of cAMP-dependent protein kinase activity in thyroid cell cultures.

The potent tumor promoter 12-O-tetradecanoyl-phorbol 13-acetate (TPA) affects several thyroid cell functions and interacts with thyroid-stimulating hormone (TSH) either by inhibiting or potentiating its action on different cellular parameters. Since phorbol ester acts mainly through the activation of protein kinase C, which is its receptor, we studied this activation and its interaction with TSH and forskolin in suspension cultures of porcine thyroid cells. In thyroid cell cultures, TPA has a dual effect on protein kinase C activity: immediately (2-5 min) after exposure of cells to TPA, it began to be translocated from the cytosol to the particulate fraction. The transfer of the cytosolic enzyme was total and could occur with or without a loss of activity. The translocated enzyme still needed Ca2+ and phospholipids for its activation. The basal activity increased transiently (2-4 h) in both the cytosol and particulate fractions during translocation. The peak activity in the particulate fraction was reached 10-30 min after exposure of cells to TPA, and was followed by down-regulation of protein kinase C and almost complete disappearance of its activity. The residual activity was about 13% of control after a 2-day exposure to TPA. It was unequally distributed between cytosol (4%) and particulate fraction (9%). Prolonged exposure of cells to TPA did not affect either the activity or the subcellular distribution of the cAMP-dependent protein kinase activity. TPA interacted with TSH and prevented the decrease of this activity induced by prolonged exposure of cells to the hormone not only when it was introduced simultaneously with TSH, but also when it was added 24 h after TSH. However, the forskolin-induced decrease in cAMP-dependent protein kinase activity was not prevented by the presence of TPA. TPA also affected the increases in cAMP accumulation mediated by TSH and forskolin. The TSH-induced increase was significantly stimulated by TPA after short contacts (5-15 min), while longer preincubations of cells with TPA provoked a very strong inhibition of the TSH action. However, the forskolin-induced stimulation of the cAMP accumulation was maintained and even further increased in the presence of TPA. Consequently, the actions of TSH and TPA are apparently interdependent, while those of forskolin and TPA seem to be parallel and independent. Neither TSH nor forskolin prevented the TPA-induced down regulation of protein kinase C. The biologically inactive phorbol ester analogue 4 alpha-phorbol 12,13-didecanoate had no effect on protein kinase C activity, and did not interact with either TSH or forskolin.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

Insulin and insulin-like growth factor 1 receptors during postnatal development of rat brain.

The binding of insulin and insulin-like growth factor 1 (IGF1) to high-affinity sites in the brain of rats aged 2-37 days was studied. Specific binding of insulin and IGF1 was assessed using tracer concentrations of 125I-insulin or 125I-IGF1. Sites for insulin and IGF1 were distinguished in these conditions as shown by competition experiments. The Kd were 3.6 nM (insulin) and 2.0 nM (IGF1). These values did not change significantly over the age range studied. The numbers of high-affinity binding sites for insulin and IGF1 were similar in adult animals. IGF1 binding was higher than the insulin binding in 2-day-old animals. The binding capacity for both insulin and IGF1 decreased from birth to age 15 and days remained stable thereafter. Tyrosine kinase activity, which is associated with these receptors, was measured using the artificial substrate poly (Glu, Tyr). It decreased over the first 15 days of life and remained stable thereafter. Autophosphorylation of the receptors confirmed this result. This decrease appears to be due to changes in the numbers of the two types of receptors, and is probably a reflection mainly of the variation in the number of IGF1 receptors. Similar results for insulin and IGF1 binding as well as tyrosine kinase activity were obtained with hypothyroid rats.

Aging↗
PubMed1988

Activation of an S6 kinase from rat astroglial cells by cAMP.

Forskolin and isoproterenol, agonists of adenylate cyclase activity, and dibutyryl cyclic AMP, stimulated an S6 kinase activity in astroglial cells. This activity was insensitive to the thermostable inhibitor of cyclic AMP-dependent protein kinase and had the same behaviour on a DEAE-Sephacel column as the mitogen stimulated S6 kinase. These observations support the idea that the cyclic AMP cascade, as well as various growth factors, can activate S6 kinase.

Animals↗
PubMed1988

Activation of adenylate cyclase in rat fat cells promotes an increase in GTP content which controls the enzyme activity.

In previous studies, we demonstrated that the treatment of adipocytes with cholera toxin or Bordetella pertussis toxin (IAP) promoted an increase in the total guanosine triphosphate (GTP) content of the cells concomitant with the increase in cyclic adenosine monophosphate (AMP) level and the resulting lipolysis. In the present studies, we show that the acute challenge of fat cells with 1 microM isoproterenol (IPNE) is associated with a transient increase in GTP level (3-fold in 6 min). This increase may be attributed to an inhibition of the disposal of GTP or to a stimulation of its synthesis. To evaluate the actual role of GTP, we used virazole, an antitumor agent which inhibits inosinic acid dehydrogenase. After 2 h preincubation of the cells with 1 mM virazole, the effect of a 6 min challenge with 1 microM IPNE is decreased by 59% at the GTP level and by 42% in cyclic AMP production. One hour later, the resulting lipolytic efficiency is reduced by 57%. IAP treatment (10 micrograms/ml) produced its maximal effect on GTP and cyclic AMP levels and on lipolysis after 90 min incubation. The antilipolytic effect of 1 microM phenylisopropyladenosine (PIA) is almost abolished. When 1 mM virazole is added to the cell suspension to deplete the guanyl nucleotide pool, the resulting lipolysis due to IAP treatment is decreased by 85%, whereas GTP and cyclic AMP levels were decreased by 80 and 70%, respectively. We can conclude that the cyclic AMP synthesis in intact cells is accompanied by a parallel increase of their GTP content, whether the stimulation results from the activation of Gs or the inhibition of Gi. The reduction of the guanyl nucleotide pool under virazole results in a relatively less important inhibition of lipolysis when Gs is stimulated than when it is Gi.

Adenosine Triphosphate↗
PubMed1988

Decrease in cAMP-dependent protein kinase activity in suspension cultures of porcine thyroid cells exposed to TSH or forskolin.

Suspension cultures of porcine thyroid cells were used to study the action of TSH and forskolin (Fk) on cAMP-dependent (PKa) and Ca2+-phospholipid-dependent (PKc) protein kinase--enzymes which represent the key step in the transduction of extracellular signals. The PKa activity in cells cultured for 2 days in the presence of TSH was decreased to about 50% of control level with a TSH dose of 0.1 mU/ml. This decrease is dose dependent; only traces of PKa activity remained at very high doses of TSH (50 mU/ml). Similar results were obtained with Fk (10(-5) M), the adenylate cyclase activator. It decreased the PKa activity to the level obtained with 0.1-1.0 mU/ml TSH. The loss of the PKa activity was parallel in cytosol and particulate fractions, suggesting that there is no translocation of enzymes under the action of either TSH or Fk. Neither TSH nor Fk had any effect on PKc, which became the predominant activity in cells exposed to either of the regulators. The cAMP-dependent phosphorylation of endogenous proteins was lower in TSH- or Fk-treated cells than in controls, and was dependent, like the PKa activity, on the dose of TSH. Polyacrylamide gel electrophoresis (PAGE) revealed the specific substrates of PKa in cultured thyroid cells. Proteins of 28, 30 and 33 kDa were regularly found, while 58 kDa protein was not present in all experiments. PAGE patterns showed that the decrease in endogenous phosphorylation in TSH- and Fk-treated cells was due to decreased labelling of PKa-specific substrates. The observed down-regulation of PKa activity could have an influence on the expression of thyroid cell differentiation.

Animals↗
PubMed1988

Properties of the 12-O-tetradecanoylphorbol-13-acetate-stimulated S6 kinase from rat astroglial cells.

The S6 kinase activity of astroglial cells in primary culture stimulated by 12-O-tetradecanoylphorbol-13-acetate (TPA) has been studied. This activity was eluted as a single peak at 0.15 M NaCl from a DEAE-Sephacel column. The chromatography of this peak on phosphocellulose revealed an activity eluted at 0.15 M NaCl. This partially purified enzyme had a sedimentation coefficient of 3.7S; Km values were 2 X 10(-5) M for ATP and 10(-6) M for 40S ribosomal subunits. The optimal Mg2+ concentration requirement was 2-3 mM. Mn2+ and Co2+ could substitute for Mg2+ (optimum concentrations 1.5 and 0.8 mM, respectively), but these cations were strong inhibitors in the presence of Mg2+. The enzyme was inhibited by N-ethylmaleimide, indicating that it contained thiol groups. This S6 kinase used ATP, but not GTP, as a phosphate donor, and exhibited great specificity for S6 as phosphate acceptor. Whole histones and protamine were slightly phosphorylated whereas phosvitin, histone H1, and surprisingly the peptide Arg-Arg-Leu-Ser-Ser-Leu-Arg-Ala were not phosphorylated. The TPA-stimulated S6 kinase resembles the insulin-, fibroblast growth factor- and cyclic AMP-stimulated enzymes, suggesting that several pathways might activate the same entity.

Adenosine Triphosphate↗
PubMed1987

The role of Ca2+ in regulating the catabolism of PAF-acether (1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine) in rabbit platelets.

In the present study we have investigated the effect of changes in the concentration of cytosolic free Ca2+ ([Ca2+]i) on the deacetylation-reacylation of PAF-acether (alkylacetylglycerophosphocholine, alkylacetyl-GPC) by rabbit platelets. Washed platelets were incubated with alkyl[3H]acetyl-GPC ([3H]acetyl-PAF) or [3H]alkylacetyl-GPC ([3H]alkyl-PAF) and [Ca2+]i was subsequently elevated by the addition of the ionophore A23187 or thrombin. The catabolism of PAF-acether was studied by measuring the release of [3H]acetate or the formation of [3H]alkylacyl-GPC. The ionophore inhibited the release of [3H]acetate and the formation of [3H]alkylacyl-GPC with no accumulation of lyso-[3H]PAF, indicating that the deacetylation of PAF-acether was blocked. The effect of ionophore on the deacetylation of PAF-acether was parallel with the increase of [Ca2+]i and could be reversed by the addition of EGTA. In contrast with the prolonged inhibition evoked by ionophore, thrombin, which induced a transient elevation of [Ca2+]i, merely delayed the deacetylation of PAF-acether. Since intact platelets failed to convert exogenous lyso-PAF, the effect of Ca2+ on its acylation was investigated by using platelet homogenates. These experiments showed that the acylation of lyso-PAF was inhibited by the exogenously added Ca2+, with a maximum effect at 1 mM. When the formation of endogenous lyso-PAF from the labelled pool of alkylacyl-GPC was examined, a prolonged increase in the concentration of lyso-PAF with a parallel and equally prolonged decrease in the cellular level of alkylacyl-GPC were observed after the addition of ionophore to intact platelets. The addition of EGTA reversed the effect of ionophore, thus permitting reacylation of lyso-PAF. In contrast, only a transient change in the level of lyso-PAF and alkylacyl-GPC was evoked by the addition of thrombin. Therefore we conclude that the inhibitory effect of Ca2+ on the deacetylation-reacylation of PAF-acether may have an important role in the regulation of its biosynthesis.

Acetates↗
PubMed1986

Activation of S6 kinase activity in astrocytes by insulin, somatomedin C and TPA.

Treatment of cultured astrocytes from 2-day-old rat cerebral hemispheres with insulin or somatomedin C (IGF1) promoted a rapid activation of a cytosolic protein kinase which phosphorylates ribosomal protein S6. Phosphorylation of substrates currently used for protein kinase assays (histone H2B and phosvitin) was not stimulated. Neither the cyclic AMP-dependent protein kinase activity nor that of protein kinase C was modified. Treatment of these astrocytes with TPA also promoted a rapid increase in S6 kinase activity in the cytosolic fraction. Simultaneously, protein kinase C disappeared from the cytosol. Neither cyclic AMP-dependent protein kinase activity nor phosvitin kinase activity was modified. The effects of insulin, IGF1 and TPA were also observed in the presence of cycloheximide. Cycloheximide also potentiated their effects. These data indicate that S6 kinase activity in astrocytes is promoted from a pre-existing molecule via the tyrosine kinase-insulin receptor and suggest that protein kinase C is implicated in the process.

Animals↗
PubMed1986

Relationships between the GTP content and the TSH-stimulated adenylate cyclase activity of cultured thyroid cells.

The adenylate cyclase activity of a crude membrane fraction derived from cells cultured for 4 days in the presence of TSH (0.1 mU/ml), when acutely stimulated with 25 mU/ml, is 5-8 times higher than that derived from control cells. It has been suggested that changes in the intracellular content of GTP resulting from TSH chronic treatment were the cause of the modified responsiveness of the cyclase. To investigate this hypothesis, a method for GTP determination was developed. The steady-state concentration of GTP in 4-day TSH-treated cells is 2-3 times higher than in 4-day control cells. The increase in GTP content is concentration dependent between 5 and 500 microU/ml TSH in the culture medium. It presents a maximum on day 4 of culture, but remains elevated up to day 5. Nevertheless the GTP content is not the only factor controlling the cyclase activity, indeed the addition of 0.1 mM GTP to membranes from control cells does not increase the response up to the level reached by membranes from TSH-treated cells. Treatment of the cells with virazole, a drug inhibiting the biosynthesis of guanyl nucleotides, greatly decreases the GTP level, but is unable to suppress the positive effect of the TSH chronic treatment on adenylate cyclase activity. These results show that the increase in GTP level resulting from culture of the cells in the presence of minute amounts of TSH is not exclusively linked to adenylate cyclase responsiveness to TSH.

Adenosine Triphosphate↗
PubMed1986

Retention of ventilatory pattern learning in normal subjects.

Two procedures for training normal subjects to increase inspiratory duration (TI) were compared. In the first procedure (feedback), a visual signal informed subjects of their TI value just after the end of each inspiration; subjects were instructed to maintain TI for a set interval previously established by the experimenter. The second procedure (pacing) consisted of delivering a periodic signal to subjects and instructing them to adjust their respiratory frequency to this signal. All subjects participated in two identical sessions, 24 h apart. Comparison of performances between the two sessions provides evidence for a retention effect in feedback subjects only, suggesting the superiority of this method. Voluntary increase of TI during training induced a spontaneous increase of tidal volume, independent of any instruction. This increase in breathing amplitude cannot be explained in terms of chemical control of breathing.

Adult↗
PubMed1986

Synchronization and knowledge of results in a ventilatory motor task.

The ability of healthy subjects to adopt a given value of inspiratory duration (TI) was examined in two different conditions: a knowledge condition in which subjects were informed of their performance on TI and synchronization of subjects' breathing rate to a periodic visual signal. The target value of TI was computed individually, by the same formula for all subjects in both procedures. 40 subjects were tested in a double-transfer design; each subject participated in two sessions 24 hr. apart. In addition to previous results showing better retention of the ventilatory task in subjects following the knowledge procedure after 24 hr., this study also shows better performance in this condition. No transfer could be evidenced, suggesting low similarity between the two tasks in spite of the fact that the resulting breathing patterns were nearly identical. The influence of the magnitude of the target on performance was also investigated.

Adult↗
PubMed1985

Tetradecanoyl phorbol-13-acetate counteracts the responsiveness of cultured thyroid cells to thyrotropin.

We have studied the effects of TPA on the metabolism of porcine thyroid cells cultured for 1-4 days in the absence (control cells) and in the presence of 0.1 mU/ml TSH (TSH cells). The phospholipid turnover, evaluated after a 2 hr incorporation of 32P-phosphate into phospholipids, is markedly modified by the presence of TPA (1.5 microM, 2 hr) in the incubation medium of control and TSH treated cells. The total incorporation is 3-4 times higher than untreated cells, the labelling of phosphatidylinositol (PI) is slightly decreased or unchanged whereas that of phosphatidylcholine (PC) is strongly increased. The increased labelling of PI, promoted by an acute TSH treatment is counteracted by TPA. This TPA effect is not observed when prelabelled cells are challenged for 5 min with the drug. A similar effect is observed when 10 nM TPA is added in the culture medium for 20 hr. The addition of TPA does not affect significantly the protein iodine content in 3 or 4 days control cells incubated for 45 min or 2 hr with 125I-iodine, but dramatically decreases the very high iodination rate of TSH cells. We have tested the TPA effect on the cyclic AMP accumulation for the last 5 min of a 2 hr incubation. TPA inhibits by about 50-80% the stimulation evoked by TSH and only by 10% that evoked by forskolin (0.1 mM). These results suggest a possible link between the PC turnover and the adenylate cyclase responsiveness to TSH and the iodination rate.

Adenylyl Cyclases↗