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Estrogen regulation of monocyte and endothelial cell adhesion
Author(s) -
Czapp Nikole,
McGuinness Michael P
Publication year - 2012
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.26.1_supplement.680.5
Subject(s) - monocyte , cell adhesion molecule , cell culture , cell adhesion , thp1 cell line , estrogen receptor , estrogen , antibody , integrin , microbiology and biotechnology , chemistry , flow cytometry , icam 1 , receptor , endothelial stem cell , cell , endocrinology , medicine , biology , immunology , in vitro , biochemistry , cancer , breast cancer , genetics
Estrogens may regulate cell adhesion molecules and alter monocyte binding to endothelial cells. These actions are mediated by receptors present in the nucleus and/or on the plasma membrane. To determine if estrogen receptors are expressed on the plasma membrane of a monocyte cell line, THP‐1 cells, were incubated in primary antibody to either ERα, ERβ, actin, or no primary antibody. A secondary antibody conjugated to metallic beads was used to isolate cells. A significantly greater number of cells were isolated with antibodies to ERα or ERβ than controls. To determine if estrogen alters levels of cell adhesion molecules HUVEC cells and THP‐1 cells were treated with 17 beta □estradiol (0–600nM) for 6, 12 and 24 hours. Western Blots were performed to measure the levels of ICAM‐1, VE‐Cad, N‐Cad, and Alpha‐L integrin. No significant differences were measured. To measure the effect of estradiol on adherence of THP‐1 cells to HUVEC cells, cell lines were treated with 200nM estradiol for 24 hours prior to co‐culture. The number of THP‐1 cells adhering to HUVECs was determined after 15 minutes of co‐culture. When HUVEC or THP‐1 were treated with 17beta estradiol there was a 2 fold decrease in the number of THP‐1cells adhering. When both HUVEC and THP‐1 cells were treated there was a 5 fold decrease in adhering THP‐1. Thus, estrogen is able to down‐regulate monocyte adhesion to endothelial cells. However, the mechanism remains unclear.