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Estrogen antagonizes LPS‐induced monocyte adhesion to endothelial cells
Author(s) -
Holm Anders,
Nilsson Bengt-Olof
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.680.4
Subject(s) - monocyte , estrogen receptor , estrogen , agonist , chemistry , lipopolysaccharide , adhesion , medicine , cell adhesion molecule , endocrinology , receptor , cell adhesion , estrogen receptor alpha , inflammation , microbiology and biotechnology , pharmacology , biology , biochemistry , organic chemistry , cancer , breast cancer
The biological actions of estrogens are supposed to be mediated by the two classical estrogen receptors ERα and ERβ, and one putative G‐protein coupled receptor, GPER1. Estrogen exerts both pro‐inflammatory and anti‐inflammatory effects but the mechanisms are not identified. Here, we investigate if estrogen affects recruitment and adhesion of monocytes to endothelial cells (EC) using a co‐culture system. The microvascular endothelial cell line bEnd.3 was incubated for 6–24 hours with lipopolysaccharide (LPS) from E. coli . Some wells were preincubated with 17β‐estradiol (E2), the ERα‐specifc agonist DPN or the ERβ‐specific agonist PPT. Adhesion of [ 3 H]‐thymidine labeled human THP‐1 monocytes to bEnd.3 was determined by measuring radioactivity of DNA from co‐culture homogenates. Preincubation with E2 reduced monocyte adhesion by about 25%, whereas preliminary results show that neither DPN nor PPT had any effect. Expression of inflammation‐associated genes, including MCP‐1, VCAM‐1 and IL‐6 was increased by LPS, but not significantly decreased by E2, DPN or PPT, suggesting that estrogen reduces adhesion to EC via another mechanism. Taken together, these data suggest that estrogen‐induced attenuation of monocyte adhesion to EC involves other molecules than MCP‐1, VCAM‐1 and IL‐6 and is mediated through another mechanism than via ERα and ERβ. Supported by the Swedish research council.