RapamycinFungusV1, Main, Exploration, bibRecord, 000972

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

Identifieur interne : 000972 ( Main/Exploration ); précédent : 000971; suivant : 000973

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

Auteurs : Thomas Bollinger [Suisse, Allemagne] ; Annalena Bollinger [Suisse] ; Sydney Gies [Allemagne] ; Lea Feldhoff [Allemagne] ; Werner Solbach [Allemagne] ; Jan Rupp [Allemagne]

Source :

Immunology and cell biology [ 1440-1711 ] ; 2016.

RBID : pubmed:26150319

Descripteurs français

English descriptors

KwdEn :
- CD4-Positive T-Lymphocytes (immunology), CD4-Positive T-Lymphocytes (metabolism), Female (MeSH), Gene Expression Regulation (MeSH), Humans (MeSH), Hypoxia-Inducible Factor 1, alpha Subunit (genetics), Hypoxia-Inducible Factor 1, alpha Subunit (metabolism), Lymphocyte Activation (immunology), Male (MeSH), Protein Stability (MeSH), RNA, Messenger (genetics), RNA, Messenger (metabolism), Transcription, Genetic (MeSH).
MESH :
- chemical , genetics : Hypoxia-Inducible Factor 1, alpha Subunit, RNA, Messenger.
- immunology : CD4-Positive T-Lymphocytes, Lymphocyte Activation.
- metabolism : CD4-Positive T-Lymphocytes, Hypoxia-Inducible Factor 1, alpha Subunit, RNA, Messenger.
- Female, Gene Expression Regulation, Humans, Male, Protein Stability, Transcription, Genetic.

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.

DOI: 10.1038/icb.2015.64
PubMed: 26150319

Affiliations:

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Le document en format XML

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<term>CD4-Positive T-Lymphocytes (metabolism)</term>
<term>Female (MeSH)</term>
<term>Gene Expression Regulation (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Hypoxia-Inducible Factor 1, alpha Subunit (genetics)</term>
<term>Hypoxia-Inducible Factor 1, alpha Subunit (metabolism)</term>
<term>Lymphocyte Activation (immunology)</term>
<term>Male (MeSH)</term>
<term>Protein Stability (MeSH)</term>
<term>RNA, Messenger (genetics)</term>
<term>RNA, Messenger (metabolism)</term>
<term>Transcription, Genetic (MeSH)</term>
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<term>ARN messager (métabolisme)</term>
<term>Activation des lymphocytes (immunologie)</term>
<term>Femelle (MeSH)</term>
<term>Humains (MeSH)</term>
<term>Lymphocytes T CD4+ (immunologie)</term>
<term>Lymphocytes T CD4+ (métabolisme)</term>
<term>Mâle (MeSH)</term>
<term>Régulation de l'expression des gènes (MeSH)</term>
<term>Sous-unité alpha du facteur-1 induit par l'hypoxie (génétique)</term>
<term>Sous-unité alpha du facteur-1 induit par l'hypoxie (métabolisme)</term>
<term>Stabilité protéique (MeSH)</term>
<term>Transcription génétique (MeSH)</term>
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<term>Sous-unité alpha du facteur-1 induit par l'hypoxie</term>
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<term>Male</term>
<term>Protein Stability</term>
<term>Transcription, Genetic</term>
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<term>Humains</term>
<term>Mâle</term>
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<term>Stabilité protéique</term>
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<front><div type="abstract" xml:lang="en">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.</div>
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<Abstract><AbstractText>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.</AbstractText>
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<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bollinger</LastName>
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</AffiliationInfo>
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</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Molecular and Clinical Infectious Diseases, University of Lübeck, Lübeck, Germany.</Affiliation>
</AffiliationInfo>
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</AffiliationInfo>
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<ForeName>Jan</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Medical Microbiology and Hygiene, University of Lübeck, Lübeck, Germany.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Molecular and Clinical Infectious Diseases, University of Lübeck, Lübeck, Germany.</Affiliation>
</AffiliationInfo>
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<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
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<MeshHeading><DescriptorName UI="D005786" MajorTopicYN="Y">Gene Expression Regulation</DescriptorName>
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	Serveur d'exploration sur la rapamycine et les champignons
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Transcription regulates HIF-1α expression in CD4(+) T cells.

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

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