Premium
EGF enhances Ca 2+ mobilization and capacitative Ca 2+ entry in mouse mammary epithelial cells
Author(s) -
Ichikawa Jun,
Furuya Kishio,
Miyata Seiji,
Nakashima Toshihiro,
Kiyohara Toshikazu
Publication year - 2000
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/1099-0844(200009)18:3<215::aid-cbf875>3.0.co;2-s
Subject(s) - epidermal growth factor , thapsigargin , medicine , endocrinology , intracellular , tyrosine kinase , biology , cell growth , immunocytochemistry , growth factor , microbiology and biotechnology , signal transduction , receptor , biochemistry
Effects of epidermal growth factor (EGF) on the intracellular Ca 2+ ([Ca 2+ ] i ) responses to nucleotides, Ca 2+ release from thapsigargin‐sensitive stores and capacitative Ca 2+ entry were investigated in cultured mouse mammary epithelial cells. EGF treatment induced proliferation of mammary epithelial cells. We checked for mitotic activity by immunocytochemistry with an anti‐PCNA (proliferating cell nuclear antigen) antibody, which stains nuclei of the cells in S‐phase of cell cycle. EGF treatment apparently increased the number of PCNA‐stained cells compared to those treated with differentiating hormones (insulin, prolactin and cortisol) or without any hormone. Application of EGF did not induce any acute [Ca 2+ ] i response. EGF treatment for 1–2 days in culture, however, enhanced [Ca 2+ ] i responses including [Ca 2+ ] i increase by ATP, UTP and other nucelotides, Ca 2+ release from thapsigargin‐sensitive stores, as well as capacitative Ca 2+ entry. Genistein, a tyrosine kinase inhibitor, prevented EGF‐induced cell proliferation and the [Ca 2+ ] i responses in a dose‐dependent manner. These results indicate that EGF treatment enhances Ca 2+ mobilization and capacitative Ca 2+ entry, well correlated with cellular proliferation in mammary epithelial cells. Copyright © 2000 John Wiley & Sons, Ltd.