Wyniki wyszukiwania

1

The effect of short-term and chronic glucocorticoid therapy on lymphocyte glucocorticoid receptor number in patients with asthma

100%

Grzanka A., Rogala B.

Archivum Immunologiae et Therapiae Experimentalis

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2003

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tom 51

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nr 5

2

Effect of some antidepressants on the low corticosterone concentration-induced gene transcription in LMCAT fibroblast cells

100%

Otczyk M., Mulik K., Budziszewska B., Jaworska-Feil L., Basta-Kaim A., Kubera M., Jagla G., Nowak W., Lason W.

Journal of Physiology and Pharmacology

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2008

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tom 59

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nr 1

The aim of the present study was to investigate effects of some classical and new antidepressants on functional activity of the glucocorticoid receceptor (GR) induced by low corticosterone concentration in mouse fibroblast cells stably transfected with mouse mammary tumor virus-chloramphenicol acetyltransferase plasmid (LMCAT cells). We found that the transcriptional activity of GR stimulated by 50 nM corticosterone was strongly attenuated by imipramine, desipramine, fluoxetine and tianeptine in a concentration-dependent way, whereas reboxetine had only a weak effect and venlafaxine was inactive. Further study revealed that the inhibitor of c-Jun N-terminal kinase - mitogen-activated protein kinase (JNK-MAPK), SP600125 (0.1 µM), reversed the imipramine-induced suppression of GR function, whereas the inhibitor of extracellular signal-regulated kinase (ERK)-MAPK, PD 98059 (15µM), potentiated the antidepressant action. No effect of selective inhibitors of p38-MAPK, phosphatidylinositol 3-kinase (PI3-K)/Akt, and glycogen synthase kinase (GSK-3) on the imipramine-induced inhibition of GR function was detected. These data indicate that the functional activity of GR evoked by low corticosterone concentration in LMCAT cells is efficiently inhibited by tricyclic antidepressants. Moreover, it was found that JNK- and ERK-MAPK were oppositely involved in the regulation of the imipramine-induced inhibition of the GR functional activity. Thus, the present study supports the notion that the interaction of antidepressants with GR may play a role in attenuating pathological hyperactivity of HPA axis in depression.

3

Glucocorticoid receptor mediates the expansion of splenic late erythroid progenitors during chronic psychological stress

84%

Vignjevic S., Budec M., Markovic D., Dikic D., Mitrovic O., Diklic M., Suboticki T., Cokic V., Jovcic G.

Journal of Physiology and Pharmacology

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2015

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tom 66

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nr 1

4

Molecular basis of mechanisms of steroid resistance in children with nephrotic syndrome

84%

Swierczewska M., Ostalska-Nowicka D., Kempisty B., Nowicki M., Zabel M.

Acta Biochimica Polonica

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2013

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tom 60

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nr 3

Steroid therapy, due to a wide range of anti-inflammatory properties of steroids, is a basic field of treatment in many human diseases including the nephrotic syndrome in children. However, not all patients respond positively to therapy which divides them into steroid sensitive (SS) and steroid resistance (SR) individuals. Many potential factors associated with steroid resistance have been identified so far. It seems that genetic factors associated with glucocorticoid receptor α (GRα), the structure of heterocomplex of GR as well as glycoprotein P or cytochrome P450 may play a role in the induction of glucocorticoid resistance. Here we described several of the molecular mechanisms, which can regulate glucocorticoid sensitivity and resistance. Moreover, we presented genetic defects, which can lead to various effects of treatment and, in a longer perspective, enable clinicians to individualize therapies.

5

Aldosterone and mineralocorticoid receptors in regulation of the cardiovascular system and pathological remodelling of the heart and arteries

84%

Sztechman D., Czarzasta K., Cudnoch-Jedrzejewska A., Szczepanska-Sadowska E., Zera T.

Journal of Physiology and Pharmacology

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2018

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tom 69

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nr 6

6

Identification and tissue distribution of a novel rat glucocorticoid receptor splice variant

84%

Ju H., Wang X., Liu Z., Liu P., Zhao Y., Xiong R., Zhou Y., Chen X.

Acta Biochimica Polonica

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2009

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tom 56

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nr 1

109-113

Glucocorticoid receptor (GR) is a steroid hormone receptor that has been shown to play important roles in diverse cellular and physiological processes. More and more evidence has revealed that the effects of glucocorticoids are mediated by the glucocorticoid receptor through genomic or nongenomic mechanisms. A growing number of glucocorticoid receptor splice variants have been identified in human tissues, but few are known in rat tissues. In this work, a novel rGR cDNA, called rGRβ, was cloned from Sprague Dawlay (SD) rat liver. Sequence analysis revealed that the rGRβ mRNA was 39 base pairs (bp) shorter than the rGR mRNA reported earlier. The deleted segment is located in exon 1 and encodes 13 repeated glutamine residues. Both the rGR and rGRβ mRNAs were quantitated by Northern blot hybridization using non-homologous glucocorticoid cDNA probes. Results showed that the rGR and rGRβ mRNAs were most abundant in the lung, the least abundant in the heart, and there were more rGR and rGRβ mRNAs in the kidney than in the liver. The identification of rGRβ may contribute to the understanding of the genomic or nongenomic effects of glucocorticoids.

7

Interference between DNA binding activities of AP-1 and GR transcription factors in rats thymocytes undergoing dexamethasone-induced apoptosis

84%

Sikora E., Rossini G. P., Grassilli E., Bellesia E., Salomoni P., Franceschi C.

Acta Biochimica Polonica

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1996

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tom 43

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nr 4

The early molecular events of glucocorticoid-induced apoptosis have been investigated by studying glucocorticoid receptor levels, as well as binding activities to GRE and AP-1 sequences, using nuclear extracts from dexamethasone (Dex)-treated rat thymocytes. When the time-course of glucocorticoid-receptor complexes in nuclei of thymocytes was evaluated by binding studies using the tritiated ligand, we found that nuclear accumulation of radioactive complexes occurred in the first hour of incubation, and was followed by a progressive decline. This trend was confirmed by immunoblotting of nuclear proteins using a monoclonal anti-glucocorticoid receptor antibody. When the kinetics of binding activity to AP-1 and GRE sequences were studied, using nuclear extracts prepared from Dex-treated thymocytes in gel shift assays, we found peaks at 1 and 2 h after Dex treatment, and a return to basal levels in the following hours. Binding specificity was proved by competition studies using non-radioactive sequences, including mutated AP-1. Unexpectedly, however, protein binding to GRE was better competed for by AP-1 sequence than by GRE itself. Data obtained using the super gel shift assay suggested that AP-l/Jun can be responsible for the high affinity for the GRE sequence. Thus, we report here for the first time that an interference between AP-1 and GR in the binding to DNA consensus sequences — previously described in other biological systems — also occurs during apoptosis induced by glucocorticoids in lymphoid cells.

8

Expression of glucocorticoid receptor and glucose transporter-1 during placental development in the diabetic rat

67%

Korgun E. T., Acar N., Sati L., Kipmen-Korgun D., Ozen A., Unek G., Ustunel I., Demir R.

Folia Histochemica et Cytobiologica

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2011

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tom 49

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nr 2

9

Biological roles of liver X receptors in immune cells

67%

Pascual-Garcia M., Valledor A. F.

Archivum Immunologiae et Therapiae Experimentalis

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2012

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tom 60

|

nr 4

10

Central corticotropin–releasing factor (CRF) may attenuate somatic pain sensitivity through involvement of glucocorticoids

67%

Yarushkina N. I., Bagaeva T. R., Filaretova L. P.

Journal of Physiology and Pharmacology

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2011

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tom 62

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nr 5

11

The decrease in JNK- and p38-MAP kinase activity is accompanied by the enhancement of PP2A phosphatase level in the brain of prenatally stressed rats

67%

Budziszewska B., Szymanska M., Leskiewicz M., Basta-Kaim A., Jaworska-Feil L., Kubera M., Jantas D., Lason W.

Journal of Physiology and Pharmacology

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2010

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tom 61

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nr 2

Our previous study suggests that in prenatal stress model of depression glucocorticoid receptor (GR) function in adult rats is enhanced. However, the long-term consequences of stress, a causal factor in depression, on intracellular elements involved into the regulation of GR function is poorly examined. Mitogen-activated protein kinases (MAPKs), activity of which is disturbed in depression, are important regulators of GR action, so they can mediate the effect of stress on GR function. Therefore, the aim of the present study was to investigate the levels of active phosphorylated forms of extracellular signal-regulated kinases (ERK), Jun N-terminal kinases (JNK) and the p38 kinase in the hippocampus and frontal cortex in rats subjected to prenatal stress. The concentration of MAP kinase phosphatase (MKP-1, MKP-2) and protein phosphatase-2A (PP2A), which dephosphorylate all forms of MAP kinases, were also determined. During verification of the applied model of depression, we found that prenatally stressed rats displayed high level of immobility in the Porsolt test and that the administration of imipramine, fluoxetine, mirtazapine and tianeptine for 21 days normalized this parameter. Western blot study revealed that rats subjected to prenatal stress had decreased levels of p-JNK1 and p-JNK2 in the hippocampus and p-p38 in the frontal cortex, but the concentrations of p-ERK1 and p-ERK2 were not changed. Chronic treatment with imipramine inhibited the stress-induced decrease in p-JNK1/2, while imipramine, fluoxetine and mirtazapine blocked changes in p-p38. PP2A phosphatase level was higher in the hippocampus and frontal cortex in prenatally stressed animals than in control rats. Chronic treatment with antidepressant drugs attenuated the stress-induced increase in the level of this phosphatase, but had no effect on its concentration in control animals. There was no significant difference in MKP-1 and in MKP-2 levels in both brain structures between control and prenatally stressed rats. The obtained results showed that prenatal stress decreased the levels of active form of JNK and p38, but enhanced PP2A phosphatase expression and most of these changes were reversed by antidepressant drugs. Since p-JNK and p-p38 are known to inhibit GR function their lowered levels may enhance glucocorticoid action. Furthermore, the increased PP2A concentration may intensify GR action not only by inhibition of JNK and p38 phosphorylation, but also by a direct influence on the process of GR translocation.

Ograniczanie wyników

The effect of short-term and chronic glucocorticoid therapy on lymphocyte glucocorticoid receptor number in patients with asthma

Effect of some antidepressants on the low corticosterone concentration-induced gene transcription in LMCAT fibroblast cells

Glucocorticoid receptor mediates the expansion of splenic late erythroid progenitors during chronic psychological stress

Molecular basis of mechanisms of steroid resistance in children with nephrotic syndrome

Aldosterone and mineralocorticoid receptors in regulation of the cardiovascular system and pathological remodelling of the heart and arteries

Identification and tissue distribution of a novel rat glucocorticoid receptor splice variant

Interference between DNA binding activities of AP-1 and GR transcription factors in rats thymocytes undergoing dexamethasone-induced apoptosis

Expression of glucocorticoid receptor and glucose transporter-1 during placental development in the diabetic rat

Biological roles of liver X receptors in immune cells

Central corticotropin–releasing factor (CRF) may attenuate somatic pain sensitivity through involvement of glucocorticoids

The decrease in JNK- and p38-MAP kinase activity is accompanied by the enhancement of PP2A phosphatase level in the brain of prenatally stressed rats