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• W2101452972 abstract "T lymphocytes are exposed to hypoxia during their development and when they migrate to hypoxic pathological sites. Although it has been shown that hypoxia inhibits Kv1.3 channels and proliferation in human T cells, the mechanisms by which hypoxia regulates T cell activation are not fully understood. Herein we test the hypothesis that hypoxic inhibition of Kv1.3 channels induces membrane depolarization, thus modulating the increase in cytoplasmic Ca 2 + that occurs during activation. Hypoxia causes membrane depolarization in human CD3 + T cells, as measured by fluorescence‐activated cell sorting (FACS) with the voltage‐sensitive dye DiBAC 4 (3). Similar depolarization is produced by the selective Kv1.3 channel blockers ShK‐Dap 22 and margatoxin. Furthermore, pre‐exposure to such blockers prevents any further depolarization by hypoxia. Since membrane depolarization is unfavourable to the influx of Ca 2 + through the CRAC channels (necessary to drive many events in T cell activation such as cytokine production and proliferation), the effect of hypoxia on T cell receptor‐mediated increase in cytoplasmic Ca 2 + was determined using fura‐2. Hypoxia depresses the increase in Ca 2 + induced by anti‐CD3/CD28 antibodies in ∼50% of lymphocytes. In the remaining cells, hypoxia either did not elicit any change or produced a small increase in cytoplasmic Ca 2 + . Similar effects were observed in resting and pre‐activated CD3 + cells and were mimicked by ShK‐Dap 22 . These effects appear to be mediated solely by Kv1.3 channels, as we find no influence of hypoxia on IKCa1 and CRAC channels. Our findings indicate that hypoxia modulates Ca 2 + homeostasis in T cells via Kv1.3 channel inhibition and membrane depolarization." @default.
• W2101452972 created "2016-06-24" @default.
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• W2101452972 date "2005-03-22" @default.
• W2101452972 modified "2023-10-16" @default.
• W2101452972 title "Hypoxia modulates early events in T cell receptor-mediated activation in human T lymphocytes via Kv1.3 channels" @default.
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• W2101452972 doi "https://doi.org/10.1113/jphysiol.2004.081893" @default.
• W2101452972 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1456048" @default.
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• W2101452972 hasPublicationYear "2005" @default.
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