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Changes in cytoplasmic calcium in endothelial cells and monocytes treated with estrogen (LB58)
Author(s) -
Baig Maarij,
Love Maia,
Phelan Doug,
Cho Ellen,
McGuinness Michael
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.lb58
Subject(s) - calcium , calcium in biology , estrogen receptor , genistein , endocrinology , cytoplasm , medicine , chemistry , signal transduction , microbiology and biotechnology , estrogen , calcium signaling , biology , cancer , breast cancer
Estrogen is a hormone which exerts its effects in different physiological processes including the initiation and progress of inflammation. In addition to nuclear receptors, estrogen binds to plasma membrane receptors and activates signal transduction pathways. This study explores the role of calcium in estrogen regulated signal transduction from the plasma membrane. For this, Human Umbilical Vein Endothelial Cells (HUVEC) and monocytes (THP‐1) were treated with estrogenic compounds (200nM) and calcium labeled using a calcium green indicator and cells were visualized and measured using confocal microscopy. In THP‐1 cells and HUVEC cells, calcium decreased in the perinuclear cytoplasm. Decreases in Calcium were measured in THP‐1 cells treated with 17β‐estradiol (16 fold), Diethylstilbestrol (DES, 4 fold), Genistein (6 fold), and Daidzein (14 fold). Similarly, decreases were observed in HUVEC cells treated with 17β‐estradiol (9 fold), DES (1 fold), Genistein (3 fold), and Daidzein (6 fold). Overall levels of intracellular calcium were not altered. Thus, the changes in perinuclear cytoplasmic calcium may be due to the movement of calcium to the plasma membrane in response to estrogen treatments.