Estrogens cause rapid activation of IP3-PKC-alpha signal transduction pathway in HEPG2 cells

Biochemical and Biophysical Research Communications
Maria MarinoAnna Trentalance

Abstract

The mechanisms through which steroids affect target cells are not fully understood. In addition to the classic model, there is now increasing evidence that steroids can exert rapid actions. It must still be elucidated if rapid and slow estrogen actions produce co-operative and/or integrative functions. The effects of estrogen on inositol trisphosphate (IP3) production and PKC-alpha levels on membrane in the HEPG2 cell line have been investigated. Results show that estrogen addition to HEPG2 cells causes a rapid increase of IP3 production. The effect was totally inhibited by pre-incubation with tyrosine-kinase inhibitor genisteine and with the anti-estrogen ICI 182,780. An increased PKC-alpha level on the membrane fraction was present 30 min after estrogen exposure. The strong signal could elicit a variety of cellular responses such as modulation of ion channel, stimulation of cell proliferation, and phosphorylation of cytosolic ER. The ability of estrogen to trigger IP3 production in human hepatoma cells is a novel aspect of estrogen action that requires the current model of hormone stimulation target cells to be revised.

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Citations

Oct 14, 2008·Genes & Nutrition·Paola Galluzzo, Maria Marino
Oct 22, 2004·Molecular Biology of the Cell·Filippo AcconciaMaria Marino
May 18, 2006·Journal of Gastroenterology and Hepatology·Matteo RicchiPaola Loria
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Aug 18, 2006·Molecular Aspects of Medicine·Paolo AscenziMaria Marino
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Mar 23, 2004·Biochemical and Biophysical Research Communications·Filippo AcconciaMaria Marino
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