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IL‐4 enhances hypoxia induced HIF‐1α protein levels in human transformed intestinal cells
Author(s) -
Scharte Marion,
Jurk Kerstin,
Kehrel Beate,
Zarbock Alexander,
Aken Hugo Van,
Singbartl Kai
Publication year - 2006
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2006.10.053
Subject(s) - hypoxia (environmental) , transcription factor , microbiology and biotechnology , immune system , hypoxia inducible factors , chemistry , transcription (linguistics) , hypoxia inducible factor 1 , biology , gene , immunology , biochemistry , oxygen , linguistics , philosophy , organic chemistry
Hypoxia‐inducible factor‐1 (HIF‐1) is a transcription factor that mediates the adaptive response to hypoxia. Increasing evidence suggests a crucial role for HIF‐1 in immune reactions. Here we investigated the effect of the Th2 type cytokines IL‐4 and IL‐10 on HIF‐1α mediated response in normoxia (21% O 2 ) and hypoxia (1% O 2 ). Incubation of human transformed intestinal cells (HT‐29) with IL‐4 significantly increased HIF‐1α protein levels during hypoxia but not during normoxia. Mechanisms involved are IL‐4 induced up‐regulation of HIF‐1α gene transcription and the PI3K signaling pathway. The increase in hypoxia‐induced accumulation of HIF‐1α protein after IL‐4 treatment did not result in up‐regulation of HIF‐1 DNA‐binding activity or HIF‐1 dependent gene expression. IL‐10 did not affect HIF‐1α protein levels.