PortalPublikationenTranscription regulates HIF-1α expression in CD4(+) T cells

Transcription regulates HIF-1α expression in CD4(+) T cells

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Transcription regulates HIF-1α expression in CD4(+) T cells. / Bollinger, Thomas; Bollinger, Annalena; Gies, Sydney; Feldhoff, Lea; Solbach, Werner; Rupp, Jan.

in: IMMUNOL CELL BIOL, Jahrgang 94, Nr. 1, 01.2016, S. 109-13.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Bollinger, T, Bollinger, A, Gies, S, Feldhoff, L, Solbach, W & Rupp, J 2016, 'Transcription regulates HIF-1α expression in CD4(+) T cells', IMMUNOL CELL BIOL, Jg. 94, Nr. 1, S. 109-13. https://doi.org/10.1038/icb.2015.64

APA

Bollinger, T., Bollinger, A., Gies, S., Feldhoff, L., Solbach, W., & Rupp, J. (2016). Transcription regulates HIF-1α expression in CD4(+) T cells. IMMUNOL CELL BIOL, 94(1), 109-13. https://doi.org/10.1038/icb.2015.64

Vancouver

Bollinger T, Bollinger A, Gies S, Feldhoff L, Solbach W, Rupp J. Transcription regulates HIF-1α expression in CD4(+) T cells. IMMUNOL CELL BIOL. 2016 Jan;94(1):109-13. https://doi.org/10.1038/icb.2015.64

Bibtex

@article{8953f7badb98428e93cd1a3a0efa5b52,
title = "Transcription regulates HIF-1α expression in CD4(+) T cells",
abstract = "The transcription factor hypoxia inducible factor-1α (HIF-1α) mediates the metabolic adaptation of cells to hypoxia and T-helper cell fate. However, HIF-1α regulation in CD4(+) T cells (T cells) remains elusive. Here we observed that depletion of oxygen (O2⩽2%) alone was not sufficient to induce HIF-1α expression in T cells. However, when hypoxic T cells were stimulated, HIF-1α was expressed and this was dependent on nuclear factor-κB- and nuclear factor of activated T cell (NFAT)-mediated transcriptional upregulation of Hif-1α mRNA. HIF-1α upregulation could be blocked by drugs inhibiting NF-κB, NFAT or mammalian target of rapamycin precluding CD4(+) T-cell stimulation or translation in T cells, as well as by blocking transcription. CD3, CD28, phorbol-12-myristat-13-acetat (PMA) or ionomycin-stimulated T cells did not express HIF-1α under normoxic conditions. In conclusion, regulation of HIF-1α expression in CD4(+) T cells in hypoxia gravely relies on its transcriptional upregulation and subsequent enhanced protein stabilization.",
keywords = "CD4-Positive T-Lymphocytes/immunology, Female, Gene Expression Regulation, Humans, Hypoxia-Inducible Factor 1, alpha Subunit/genetics, Lymphocyte Activation/immunology, Male, Protein Stability, RNA, Messenger/genetics, Transcription, Genetic",
author = "Thomas Bollinger and Annalena Bollinger and Sydney Gies and Lea Feldhoff and Werner Solbach and Jan Rupp",
year = "2016",
month = jan,
doi = "10.1038/icb.2015.64",
language = "English",
volume = "94",
pages = "109--13",
journal = "IMMUNOL CELL BIOL",
issn = "0818-9641",
publisher = "John Wiley & Sons",
number = "1",

}

RIS

TY - JOUR

T1 - Transcription regulates HIF-1α expression in CD4(+) T cells

AU - Bollinger, Thomas

AU - Bollinger, Annalena

AU - Gies, Sydney

AU - Feldhoff, Lea

AU - Solbach, Werner

AU - Rupp, Jan

PY - 2016/1

Y1 - 2016/1

N2 - The transcription factor hypoxia inducible factor-1α (HIF-1α) mediates the metabolic adaptation of cells to hypoxia and T-helper cell fate. However, HIF-1α regulation in CD4(+) T cells (T cells) remains elusive. Here we observed that depletion of oxygen (O2⩽2%) alone was not sufficient to induce HIF-1α expression in T cells. However, when hypoxic T cells were stimulated, HIF-1α was expressed and this was dependent on nuclear factor-κB- and nuclear factor of activated T cell (NFAT)-mediated transcriptional upregulation of Hif-1α mRNA. HIF-1α upregulation could be blocked by drugs inhibiting NF-κB, NFAT or mammalian target of rapamycin precluding CD4(+) T-cell stimulation or translation in T cells, as well as by blocking transcription. CD3, CD28, phorbol-12-myristat-13-acetat (PMA) or ionomycin-stimulated T cells did not express HIF-1α under normoxic conditions. In conclusion, regulation of HIF-1α expression in CD4(+) T cells in hypoxia gravely relies on its transcriptional upregulation and subsequent enhanced protein stabilization.

AB - The transcription factor hypoxia inducible factor-1α (HIF-1α) mediates the metabolic adaptation of cells to hypoxia and T-helper cell fate. However, HIF-1α regulation in CD4(+) T cells (T cells) remains elusive. Here we observed that depletion of oxygen (O2⩽2%) alone was not sufficient to induce HIF-1α expression in T cells. However, when hypoxic T cells were stimulated, HIF-1α was expressed and this was dependent on nuclear factor-κB- and nuclear factor of activated T cell (NFAT)-mediated transcriptional upregulation of Hif-1α mRNA. HIF-1α upregulation could be blocked by drugs inhibiting NF-κB, NFAT or mammalian target of rapamycin precluding CD4(+) T-cell stimulation or translation in T cells, as well as by blocking transcription. CD3, CD28, phorbol-12-myristat-13-acetat (PMA) or ionomycin-stimulated T cells did not express HIF-1α under normoxic conditions. In conclusion, regulation of HIF-1α expression in CD4(+) T cells in hypoxia gravely relies on its transcriptional upregulation and subsequent enhanced protein stabilization.

KW - CD4-Positive T-Lymphocytes/immunology

KW - Female

KW - Gene Expression Regulation

KW - Humans

KW - Hypoxia-Inducible Factor 1, alpha Subunit/genetics

KW - Lymphocyte Activation/immunology

KW - Male

KW - Protein Stability

KW - RNA, Messenger/genetics

KW - Transcription, Genetic

U2 - 10.1038/icb.2015.64

DO - 10.1038/icb.2015.64

M3 - SCORING: Journal article

C2 - 26150319

VL - 94

SP - 109

EP - 113

JO - IMMUNOL CELL BIOL

JF - IMMUNOL CELL BIOL

SN - 0818-9641

IS - 1

ER -