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C Calle

Publications and source records attributed to C Calle.

At least 19 recordsLinked to original sources
PubMed2002

Transcriptional activation of the human insulin receptor gene by 1,25-dihydroxyvitamin D(3).

Treatment with 10(-8) M 1,25-dihydroxyvitamin D(3) for 24 h causes transcriptional activation of the human insulin receptor gene in U-937 human promonocytic cells. The activation seems to potentiate the response to insulin in terms of glucose oxidation. Wortmannin, a phosphatidylinositol 3-kinase inhibitor, causes a greater inhibition of insulin-stimulated glucose oxidation in 1,25-dihydroxyvitamin D(3)-treated cells than in untreated cells. This suggests a stimulation of phosphatidylinositol 3-kinase activity by 1,25-dihydroxyvitamin D(3), which could mediate, at least in part, the potentiation of the insulin response.

Androstadienes↗
PubMed2002

Aldosterone impairs insulin responsiveness in U-937 human promonocytic cells via the downregulation of its own receptor.

In an earlier study, we have reported an inhibition of insulin receptor (IR) mRNA levels and insulin binding by aldosterone in U-937 human promonocytic cells. In the present extension of our studies, we demonstrate that this inhibition by aldosterone had no effects on basal glucose transport or on basal thymidine incorporation into DNA, while the cell responsiveness reflected by the maximal response to insulin was decreased by 23% for glucose transport and by 31% for DNA synthesis after the aldosterone treatment. We also prove that this inhibition of the insulin response by aldosterone is mediated by a downregulation of the levels of mineralocorticoid receptors (MRs) (50% decrease) and their mRNA (50% decrease). In addition, the mineralocorticoid antagonist spironolactone reversed the decrease in MR mRNA levels elicited by aldosterone, which suggests the involvement of this receptor in the process.

Aldosterone↗
PubMed2000

Etoposide stimulates 1,25-dihydroxyvitamin D3 differentiation activity, hormone binding and hormone receptor expression in HL-60 human promyelocytic cells.

The simultaneous administration of the DNA topoisomerase II inhibitor etoposide (0.15 mM) and 1,25-dihydroxyvitamin D3 (VD3) (10 nM) synergistically induced the differentiation of HL-60 human promyelocytic leukemia cells. Similar results were obtained using U-937 human promonocytic cells, or the topoisomerase II inhibitors doxorubicin (15 nM) and mitoxantrone (2.5 nM). When sequential treatments were used, pre-incubation with VD3 had little effect on the subsequent action of etoposide, while pre-incubation with etoposide greatly potentiated the subsequent action of VD3. In addition, etoposide treatment stimulated VD3 binding activity and increased VD3 receptor mRNA and protein levels. The increase in hormone receptor expression may explain, at least in part, the capacity of topoisomerase inhibitors to potentiate the differentiation inducing activity of VD3.

Apoptosis↗
PubMed2000

Stimulation by 1,25-dihydroxyvitamin D3 of insulin receptor expression and insulin responsiveness for glucose transport in U-937 human promonocytic cells.

In the present work, we demonstrate that treatment with 1,25-dihydroxyvitamin D3 for 24 hours increased in a dose-dependent manner the levels of the two major insulin receptor (IR) mRNAs (11 and 8.5 Kb) present in U-937 human promonocytic cells. These levels reached maximum values (1.8-fold 11 Kb; 1.4-fold 8.5 Kb) with the addition of 10(-8) M 1,25-dihydroxyvitamin D3. In these optimal conditions the stimulatory effect of 1,25-dihydroxyvitamin D3 was accompanied by increases in both IR capacity, and insulin responsiveness for glucose transport in these cells. Moreover, such increases appear to be mediated by an enhanced expression of the receptor for 1,25-dihydroxyvitamin D3, measured at the level of both RNA and protein. These results provide evidence of 1,25-dihydroxyvitamin D3 acting as genomic stimulator of the insulin response in the control of glucose transport.

Calcitriol↗
PubMed1998

In vivo tissue specific modulation of rat insulin receptor gene expression in an experimental model of mineralocorticoid excess.

Insulin receptor (IR) gene expression at the mRNA level was investigated in hindlimb skeletal muscle, epididymal adipose tissue and in the liver of rats exposed to prolonged in vivo administration of deoxycorticosterone acetate (DOCA). Following treatment, plasma insulin levels were reduced while glucose levels increased compared to values in control rats. DOCA-treated animals showed an increase in blood pressure and a reduction in body weight. This treatment also induced hypokalemia and decreased plasma protein levels. Sodium levels were unaffected. Moreover, no differences in DNA and protein content or in the indicator of cell size (protein/DNA) were observed in the skeletal muscle or adipose tissue of animals. In contrast, there was a clear increase in the protein and DNA contents of the liver with no change in the indicator of cell size. Northern blot assays revealed 2 major IR mRNA species of approximately 9.5 and 7.5 Kb in the 3 tissues from control animals. DOCA treatment induced no change in the levels of either RNA species in skeletal muscle. However, a decrease of approximately 22% was detected in the levels of both species in adipose tissue whereas the liver showed an increase of 64%. These results provide the first evidence for an in vivo tissue-specific modulation of IR mRNA levels under experimental conditions of mineralocorticoid excess.

Adipose Tissue↗
PubMed1998

Epinephrine-induced reduction in insulin receptor mRNA level and stability in U-937 human promonocytic cells.

The administration of 10(-5) M epinephrine transiently decreased insulin receptor (IR) mRNA levels in U-937 human promonocytic cells, which reached their minimum value after 24 hours. Such a decrease seems to be due, at least in part, to a reduction in transcript stability, since the IR mRNA half-life was observed to decline from approximately 4h in untreated cells to 3 h in epinephrine-treated cells. Computer inspection of the sequence of the 3' untranslated region of the human IR mRNA showed nine AUUUA pentamers and three U-rich regions. These domains could be targets for a RNA-binding protein induced by treatment with epinephrine producing a destabilization of IR mRNA in U-937 cells.

Blotting, Northern↗
PubMed1997

Tissue-specific modulation of insulin receptor mRNA levels in adrenaline-treated rats.

Insulin receptor (IR) gene expression at the mRNA level was investigated in liver, hindlimb skeletal muscle, and epididymal adipose tissue of rats exposed to prolonged in vivo administration of adrenaline in relation to control rats. In the liver of adrenaline-treated rats, there were no differences in relation to controls when DNA and protein content were measured. In skeletal muscle, only a slight decrease in protein concentration was detected. By contrast, a clear increase in both protein and DNA content was observed in the adipose tissue of treated animals. Northern blot assays revealed two IR mRNA species of approximately 9.5 and 7.5 Kb in the three tissues from controls. Adrenaline treatment induced an increase of approximately 60% in the levels of both RNAs in adipose tissue but not in liver or skeletal muscle. These results provide evidence for an in vivo tissue-specific regulation of IR gene expression at the mRNA level in rats under an experimental condition of excess of catecholamines.

Adipose Tissue↗
PubMed1997

Heat-shock and cadmium chloride increase the vimentin mRNA and protein levels in U-937 human promonocytic cells.

Heat-shock for 2 hours at 42 degrees C, or the administration for 3 hours of 100 or 150 microM cadmium chloride, inhibited the subsequent proliferation activity, induced the expression of functional differentiation markers, and caused an increase in the amount of the stress-responsive HSP70 protein in U-937 human promonocytic cells. In addition, both heat and cadmium produced an increase in the amount of the intermediate filament protein vimentin, as determined by immunoblot and immunofluorescence assays. By contrast, the amounts of actin and beta-tubulin were not significantly altered. The amount of vimentin mRNA was also increased during recovery from stress, indicating that vimentin expression was not exclusively regulated at the protein level. Although cadmium caused an early, transient stimulation of c-jun and c-fos expression and AP-1 binding activity, heat-shock failed to alter both protooncogene expression and transcription factor binding, indicating that the stress-induced vimentin increase was not the result of AP-1-mediated transcriptional activation. Finally, it was observed that the rate of decay of vimentin mRNA upon actinomycin D administration was decreased in heat- and cadmium-pretreated cells in comparison to untreated cells. These results indicate that stress treatments cause an increase in vimentin levels in promonocytic cells, which may be explained at least in part by transcript stabilization.

Actins↗
PubMed1996

Effect of dexamethasone on insulin receptor mRNA levels, RNA stability and isotype RNA pattern in U-937 human promonocytic cells.

The administration of 5 x 10(-6) mol/l dexamethasone transiently increased insulin receptor (IR) mRNA levels in U-937 human promonocytic cells, which reached the maximum level at 15 h of treatment. Dexamethasone treatment did not affect the IR mRNA half-life (approximately 4 h), suggesting that the increase is regulated at the transcriptional level. The stimulatory action of dexamethasone was not prevented by the simultaneous presence of the protein synthesis inhibitor cycloheximide, indicating that the induction of IR gene transcription occurs as a direct response to the action of the synthetic glucocorticoid. Finally, the A isoform (lacking exon 11) was found to be the only IR isoform present in both untreated and dexamethasone treated-U-937 cells.

Cell Line↗
PubMed1995

The effect of 1,25-dihydroxyvitamin D3 on insulin binding, insulin receptor mRNA levels, and isotype RNA pattern in U-937 human promonocytic cells.

We have studied the effect of 10(-8) M 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] on insulin binding, insulin receptor gene expression, and isotype mRNA pattern in U-937 human promonocytic cells. Binding assays indicated that 1,25-(OH)2D3 increased total receptor number without altering receptor affinity, while the dissociation rate of the hormone bound to its receptor remained unchanged. RNA blot assays indicated that 1,25-(OH)2D3 increased the levels of the two major insulin receptor mRNAs (11 and 8.5 kb) present in these cells. Experiments with the RNA synthesis inhibitor actinomycin D suggested that 1,25-(OH)2D3 did not alter the stability of total insulin receptor mRNA. Experiments with the protein synthesis inhibitor cycloheximide indicated that the increase in the amounts of this mRNA occurs as a direct response to the action of the hormone. Finally, polymerase chain reaction assays revealed that the insulin receptor mRNA isotype lacking the exon 11 (A isotype) was the only one present in both untreated and 1,25-(OH)2D3-treated U-937 cells. This indicates that 1,25-(OH)2D3 does not alter the splicing of the primary insulin receptor transcript in this cell line.

Base Sequence↗
PubMed1995

Modulation of HSP70 and HSP27 gene expression by the differentiation inducer sodium butyrate in U-937 human promonocytic leukemia cells.

The treatment of U-937 human promonocytic cells with the differentiation inducer sodium butyrate (0.75 mM) transiently increased heat-shock protein 70 (HSP70) mRNA levels between 3 and 6 h, and heat-shock protein 27 (HSP27) mRNA levels between 12 and 24 h, as indicated by northern blot assays. Gel retardation assays indicated that butyrate also stimulated heat-shock factor (HSF) binding activity between 3 and 6 h, suggesting that the activation of HSP70 gene expression was mediated by the heat-shock factor DNA response element (HSE). In addition, the treatment provoked a biphasic alteration of the c-fos mRNA level, consisting of a slight increase between 0.5 and 3 h followed by a greater increase between 12 and 48 h, while it caused a single increase between 12 and 48 h in c-jun mRNA level. The possible involvement of the heat-shock protein genes in the butyrate-induced differentiation of U-937 cells is discussed.

Base Sequence↗
PubMed1995

cAMP increasing agents prevent the stimulation of heat-shock protein 70 (HSP70) gene expression by cadmium chloride in human myeloid cell lines.

Treatment of U-937 human promonocytic cells with the cAMP increasing agents isoproterenol plus theophylline decreased the basal level of heat-shock protein 70 (HSP70) mRNA. In addition, the cAMP increasing agents attenuated the increase in HSP70 mRNA and protein levels produced by cadmium chloride in U-937 and other human myeloid cell lines, reduced the capacity of cadmium treatment to generate stress-tolerance, and attenuated the cadmium-produced stimulation of heat-shock factor (HSF) binding activity. By contrast, isoproterenol plus theophylline failed to attenuate the stimulation of HSP70 gene expression and HSF binding activity caused by heat-shock. Isoproterenol plus theophylline did not prevent the uptake of cadmium into the cells, and increased to a similar extent the intracellular cAMP levels in cadmium- and heat-treated cells. The cAMP increasing agents reduced the induction by cadmium of the HSP27 stress gene, but failed to attenuate other cadmium-elicited stress reactions such as the inhibition of total protein synthesis. It is concluded that cAMP does not inhibit the stress response as a whole, but it interferes with some step of the pathway by which cadmium specifically stimulates HSF binding activity and as a consequence HSP70 gene expression, in human myeloid cell lines.

Base Sequence↗
PubMed1994

Tissue-specific changes in insulin receptor mRNA concentrations in dexamethasone-treated and adrenalectomized rats.

The relative concentrations of total insulin receptor (IR) mRNA were measured in the epididymal adipose tissue and liver of intact untreated rats, dexamethasone-treated rats, adrenalectomized rats and adrenalectomized rats treated with dexamethasone, using RNA blot assays and a specific IR cDNA probe. Northern blot assays revealed two IR mRNA species of approximately 9.5 and 7.5 kb, in both tissues. Dot-Blot assays followed by densitometry indicated that dexamethasone induced an approximately three-fold increase in IR mRNA in liver, but not in epididymal adipose tissue. By contrast, neither adrenalectomy alone nor the combination of adrenalectomy plus dexamethasone treatment altered the IR mRNA concentrations in liver nor in adipose tissue, which indicates that adrenalectomy was able to prevent the stimulation of IR gene expression caused by dexamethasone in rat liver. These results provide evidence for an "in vivo" tissue-specific regulation of IR gene expression, at the mRNA level, in rats under experimental conditions of an excess or insufficiency of glucocorticoids.

Adipose Tissue↗
PubMed1993

Identification of glucagon receptors in human adipocytes from a liposarcoma.

The presence of glucagon receptors on human adipocytes has not yet been described. In this work we present an exceptional case of glucagon binding to human adipocytes taken from a malignant tumor of adipose tissue of a patient with a liposarcoma. Binding analysis revealed that the total number of glucagon receptors on liposarcoma-cells was 99,000 and the apparent receptor affinity (ED:50) was 5 x 10(-9) M. Despite the presence of these specific receptors, glucagon was unable to induce a lipolytic response, or to activate the adenylate-cyclase system in these liposarcoma-cells. Whether the induction of glucagon receptors is a specific process of the tumor biology remains to be elucidated.

Adipose Tissue↗
PubMed1993

Tissue-specific modulation of insulin receptor mRNA levels in a patient with a phaeochromocytoma.

We have observed that the expression of the insulin-receptor gene is regulated in a tissue-specific manner in a patient with a phaeochromocytoma. Our results indicate that insulin receptor mRNA levels are decreased in adipose tissue and increased in both liver and skeletal muscle as compared with the corresponding values in the same tissues of a control patient. These findings provide the first evidence that insulin receptor mRNA levels may be modulated in vivo by high levels of catecholamines.

Adipose Tissue↗
PubMed1992

Modulation by dexamethasone of insulin binding and insulin receptor mRNA levels in U-937 human promonocytic cells.

Treatment with 5 x 10(-6) M dexamethasone stimulated insulin binding in human promonocytic U-937 cells. When curvilinear Scatchard plots were examined according to the one-site model, only changes in affinity, but not in receptor numbers, were observed. However, when the two-site model was applied, an increase in both the affinity and the number of the high affinity-low capacity sites was observed, with maximum values at 15 h. By contrast, the low affinity-high capacity sites did not undergo significant alterations. Northern blot assays revealed two insulin receptor-related mRNAs of approximately 11 and 7 kb in size. Dexamethasone increased the levels of these RNAs, following similar kinetics to those of high affinity receptor expression. This suggests that the 11 and 7 kb species carry information for high affinity insulin receptors, and that in U-937 cells the expression of this receptor subclass is primarily regulated at the mRNA level.

Cell Line↗
PubMed1992

[Changes in the mechanism of action of insulin on fatty tissue accumulations in lipomas, Madelung's lipomatosis and liposarcoma].

In this paper, the preliminary results regarding the alterations of the biological action mechanism of insulin in several types of pathological accumulations of fat, i.e. lipomas, Madelung's Lipomatosis and liposarcoma, are presented. The results indicate significant alterations both at the insulin receptor and post-receptor levels, with reduced biological activity of this hormone, which could have and inductive role in the pathogenesis of such entities.

Adipose Tissue↗