Relevance of nuclear receptor expression in a Tchreg cell line, HOZOT: RXRα and PPARγ negatively regulate IFN-γ production

Abstract Objectives. Bisphenol A (BPA), as an indispensable plastic additive, has also been proven as an endocrine disruptor associated with adverse health effects including impaired ovarian function and cancer. Due to the restrictions of its usage, several analogs have been employed to replace BPA. Although many studies revealed a harmfulness in the biological effects of BPA analogs, their specific targets remain largely unknown. Nuclear receptors (NRs) may be one of the most important targets of bisphenols. Therefore, in this study, our attention was directed to explore the effect of BPA and its analogs, AF and S, on the mRNA expression of selected NRs involved in the steroidogenic and carcinogenic pathways in the human granulosa cell line COV434. The NRs investigated included: thyroid hormone receptor α (THRA), peroxisome proliferator activating receptor β/δ (PPARD), retinoid X receptor α (RXRA), chicken ovalbumin upstream promoter-transcription factor II (COUPTFII), nuclear receptor-related protein 1 (NURR1), and liver receptor homolog-1 (LRH1). Methods. COV434 cells were treated with the bisphenols at the concentrations of 10−9 M, 10−7 M, and 10−5 M, and after 24 and 48 h, cell viability was monitored by the MTS assay and gene expressions were analyzed using RT-qPCR. Results. Bisphenol treatment did not alter the COV434 cell viability. After 24 h, the expression of neither of the NRs was changed. Likewise, after 48 h, the expression of the selected genes was not altered. However, both BPAF and BPS increased, at the highest concentration (10−5 M) used, the mRNA levels of both PPARD and NURR1 NRs after 48 h of the treatment. In the BPA-treated groups, no significant upregulation was observed. Conclusions. In the present study, the effect of bisphenols on COUP-TFII, Nurr1, and LRH-1 NRs was investigated for the first time. Although generally we did not observe that BPs provoked any alterations in the expression of the selected NRs in COV434 cells, at specific concentrations and time points they might alter mRNA expression of certain NRs (NURR1, PPARD).

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Chemokine and Chemokine Receptor Expression in a Novel Human Mesangial Cell Line

Journal of the American Society of Nephrology ◽

10.1681/asn.v10112314 ◽

1999 ◽

Vol 10 (11) ◽

pp. 2314-2322

Author(s):

BERNHARD BANAS ◽

BRUNO LUCKOW ◽

MARCUS MÖLLER ◽

CHRISTIANE KLIER ◽

PETER J. NELSON ◽

...

Keyword(s):

Cell Line ◽

Chemokine Receptor ◽

Chemokine Receptors ◽

Mesangial Cell ◽

Mesangial Cells ◽

Receptor Expression ◽

Rnase Protection ◽

Chemokine Receptor Expression ◽

Tnf Α ◽

Ifn Γ

Abstract. Chemokines are thought to play a pivotal role in mediating the selective migration of leukocytes into sites of tissue injury. The local production of chemokines by mesangial cells (MC) has been linked to inflammatory processes within the glomerulus. To study the chemokine biology of human MC, an immortalized human MC line was generated and then chemokine and chemokine receptor expression was examined in response to various proinflammatory stimuli. The results show that human MC have a specific and limited repertoire of chemokine expression. The stimulus-specific regulation of the chemokines monocyte chemoattractant protein-1 (MCP-1), regulated upon activation, normal T cell expressed and secreted (RANTES), interleukin-8 (IL-8), and IP-10 was demonstrated using RNase protection assays. Transcripts for the chemokines MIP-1α, MIP-1β, I-309, or lymphotactin could not be detected. The expression of CC chemokine receptors was investigated by reverse transcription-PCR and RNase protection assays. MC stimulated with interferon-γ (IFN-γ) expressed mRNA for the chemokine receptor CCR1. The expression could be further increased by activating the cells with a combination of tumor necrosis factor-α (TNF-α), IL-1β, and IFN-γ. Under these conditions, no mRNA for CCR2, CCR3, CCR4, CCR5, or CCR8 was detected. A comparison of the immortalized human mesangial cells with primary cells showed identical expression patterns of chemokine receptors. To demonstrate functional activity of chemokine receptors expressed by human MC, chemotaxis assays were performed. MC stimulated with a combination of TNF-α, IL-1β, and IFN-γ, but not unstimulated MC, migrated toward a RANTES gradient. Eotaxin did not enhance the migratory activity of human MC. In summary, a novel human mesangial cell line was established and the pattern of chemokine expression was examined. For the first time, the inducible expression of functionally active CCR1 by human MC was shown.

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Leptin receptor expression in the human erythroleukemia cell line K562

Aktuelle Ernährungsmedizin ◽

10.1055/s-2003-816373 ◽

2003 ◽

Vol 28 (05) ◽

Author(s):

C Peiser ◽

K Hupe-Sodmann ◽

RE Lang

Keyword(s):

Cell Line ◽

Leptin Receptor ◽

Receptor Expression ◽

Erythroleukemia Cell

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Faculty Opinions recommendation of Nuclear receptor expression links the circadian clock to metabolism.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1044139.494054 ◽

2006 ◽

Author(s):

Michael Müller

Keyword(s):

Circadian Clock ◽

Nuclear Receptor ◽

Receptor Expression

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Differently labeled peptide ligands for rapid investigation of receptor expression on a new human glioblastoma cell line

Peptides ◽

10.1016/s0196-9781(00)00328-4 ◽

2000 ◽

Vol 21 (12) ◽

pp. 1885-1893 ◽

Cited By ~ 13

Author(s):

Marlies Fabry ◽

Chiara Cabrele ◽

Hartwig Höcker ◽

Annette G Beck-Sickinger

Keyword(s):

Cell Line ◽

Peptide Ligands ◽

Receptor Expression ◽

Glioblastoma Cell Line ◽

Glioblastoma Cell ◽

Human Glioblastoma ◽

Human Glioblastoma Cell Line ◽

Human Glioblastoma Cell

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Downregulation of c-kit (Stem Cell Factor Receptor) in Transformed Hematopoietic Precursor Cells by Stroma Cells

Blood ◽

10.1182/blood.v93.2.554 ◽

1999 ◽

Vol 93 (2) ◽

pp. 554-563 ◽

Cited By ~ 5

Author(s):

Christoph Heberlein ◽

Jutta Friel ◽

Christine Laker ◽

Dorothee von Laer ◽

Ulla Bergholz ◽

...

Keyword(s):

Stem Cell ◽

Cell Line ◽

Stem Cell Factor ◽

Progenitor Cell ◽

Receptor Expression ◽

General Mechanism ◽

Ligand Interaction ◽

Kit Ligand ◽

Kit Receptor ◽

Progenitor Cell Line

Abstract We show a dramatic downregulation of the stem cell factor (SCF) receptor in different hematopoietic cell lines by murine stroma. Growth of the human erythroid/macrophage progenitor cell line TF-1 is dependent on granulocyte-macrophage colony-stimulating factor (GM-CSF) or interleukin-3 (IL-3). However, TF-1 cells clone and proliferate equally well on stroma. Independent stroma-dependent TF-1 clones (TF-1S) were generated on MS-5 stroma. Growth of TF-1S and TF-1 cells on stroma still requires interaction between c-kit (SCF receptor) and its ligand SCF, because antibodies against c-kit inhibit growth to less than 2%. Surprisingly, c-kit receptor expression (RNA and protein) was downregulated by 2 to 3 orders of magnitude in TF-1S and TF-1 cells grown on stroma. This stroma-dependent regulation of the kit receptor in TF-1 was also observed on exposure to kit ligand-negative stroma, thus indicating the need for heterologous receptor ligand interaction. Removal of stroma induced upregulation by 2 to 4 orders of magnitude. Downregulation and upregulation of c-kit expression could also be shown for the megakaryocytic progenitor cell line M-07e and was comparable to that of TF-1, indicating that stroma-dependent regulation of c-kit is a general mechanism. Downregulation may be an economic way to compensate for the increased sensitivity of the c-kit/ligand interaction on stroma. The stroma-dependent c-kit regulation most likely occurs at the transcriptional level, because mechanisms, such as splicing, attenuation, differential promoter usage, or mRNA stability, could be excluded.

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A GM-colony-stimulating factor (CSF) activated ribonuclease system transregulates M-CSF receptor expression in the murine FDC-P1/MAC myeloid cell line.

Molecular Biology of the Cell ◽

10.1091/mbc.3.5.535 ◽

1992 ◽

Vol 3 (5) ◽

pp. 535-544 ◽

Cited By ~ 4

Author(s):

B C Gliniak ◽

L S Park ◽

L R Rohrschneider

Keyword(s):

Protein Synthesis ◽

Cell Line ◽

Transcriptional Activation ◽

Mrna Degradation ◽

Receptor Expression ◽

Metabolic Inhibitors ◽

Colony Stimulating Factor ◽

Gm Csf ◽

Stimulating Factor

The murine myeloid precursor cell line FDC-P1/MAC simultaneously expresses receptors for multi-colony-stimulating factor (CSF), granulocyte-macrophage (GM)-CSF, and macrophage (M)-CSF. Growth of FDC-P1/MAC cells in either multi-CSF or GM-CSF results in the posttranscriptional suppression of M-CSF receptor (c-fms proto-oncogene) expression. We use the term transregulation to describe this control of receptor expression and have further characterized this regulatory process. The removal of FDC-P1/MAC cells from GM-CSF stimulation resulted in the re-expression of c-fms mRNA independent of M-CSF stimulation and new protein synthesis. Switching FDC-P1/MAC cells from growth in M-CSF to GM-CSF caused the selective degradation of c-fms mRNA within 6 h after factor switching. Blocking protein synthesis or gene transcription with metabolic inhibitors effectively prevented GM-CSF stimulated degradation of c-fms mRNA. These results suggest that the transregulation of c-fms transcripts by GM-CSF requires the transcriptional activation of a selective mRNA degradation factor. In vitro analysis, the use of cytoplasmic cell extracts, provided evidence that a ribonuclease is preferentially active in GM-CSF stimulated cells, although the specificity for mRNA degradation in vitro is broader than seen in vivo. Together, these data suggest that GM-CSF can dominantly transregulate the level of c-fms transcript through the transcriptional activation of a ribonuclease degradation system.

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