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Estradiol binding to cell surface raises cytosolic free calcium in T cells

MPG-Autoren
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Giese,  Günter
Department of Biomedical Optics, Max Planck Institute for Medical Research, Max Planck Society;
Light Microscopy Facility, Max Planck Institute for Medical Research, Max Planck Society;

Externe Ressourcen

http://www.sciencedirect.com/science/article/pii/S0014579398000398/pdfft?md5=b8fb7cbc15d166f29552f77a1444d03f&pid=1-s2.0-S0014579398000398-main.pdf
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https://doi.org/10.1016/S0014-5793(98)00039-8
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Zitation

Benten, W. P. M., Lieberherr, M., Giese, G., & Wunderlich, F. (1998). Estradiol binding to cell surface raises cytosolic free calcium in T cells. FEBS Letters, 422(3), 349-353. doi:10.1016/S0014-5793(98)00039-8.


Zitierlink: https://hdl.handle.net/11858/00-001M-0000-0019-A4C9-8
Zusammenfassung
The Fura−2 method is used to examine a possible action of 17β−estradiol (E2) on [Ca2+]i of splenic T cells isolated from female C57BL/10 mice. E2 concentrations between 10 fM and 10 nM induce a rapid and dose−dependent increase in [Ca2+]i due to Ca2+ influx and release of Ca2+ from intracellular stores. Ca2+ influx is mediated by Ca2+ channels which are completely blockable by Ni2+ and partly by nifedipine. The antiestrogen tamoxifen does not inhibit the E2−induced rise in [Ca2+]i. Ca2+ influx and Ca2+ release from intracellular stores is also inducible by plasma membrane impermeable E2 conjugated to BSA. E2−BSA−FITC binds to the surface of T cells of both the CD4+ and CD8+ subset. Our data suggest a novel E2−signalling pathway in T cells which is not mediated through the classical nuclear estrogen receptor response but rather through putative plasma membrane receptors for E2