Abstract
The purpose of this study was to test the hypothesis that specific macrophage-secreted cytokines cause gene expression changes in endometrial stromal cells that reproduce the effects of macro-phages in the development of endometriosis. Telomerase-immortalized human endometrial stromal cells (T-HESC) were treated with tumor necrosis factor α (TNFα, 5 ng/ml) and interleukin 1β (IL1β, 1 ng/ml). Differential expression of 249 genes was identified by DNA microarray. Ontologies such as peptidases, cell adhesion, cell death/cell cycle, growth factors, cytoskeletal organization, defense/immune system, signal transduction, and transcriptional regulation which are related to the development of endometriosis were represented by these genes. The up-regulation of interleukin 8 (IL8), interleukin 6 (IL6), IL1β and matrix metallopro-teinase 3 (MMP3) in response to TNFα ± ILIβ in T-HESC cells was confirmed by real time RT-PCR. TNFα ± ILIβ did not affect the migration or invasion of T-HESC cells. This study reinforces our previous investigations on communication between cells of the immune system and endometrial stromal cells and their potential role in the development of endometriosis.
Highlights
Endometriosis is an inflammatory disease in which endometrial tissue implants and grows outside the uterus [1]
In the current project we tested the hypothesis that specific cytokines and growth factors secreted by macrophages (tumor necrosis factor α (TNFα), interleukin 1β (IL1β), interleukin 6 (IL6), and interleukin 8 (IL8), and the growth factor, transforming growth factor β (TGFβ)) cause gene expression changes in telomerase-immortalized human endometrial stromal cells (T-HESC) cells that reproduce the effects of macrophage conditioned medium
Concentration-response curves were carried out to identify the concentrations of TNFα, IL1β, TGFβ, IL8, and IL6 that achieved the best response from cultured endometrial stromal cells
Summary
Endometriosis is an inflammatory disease in which endometrial tissue implants and grows outside the uterus [1]. Factors secreted by macrophages and other immune system cells that are implicated in the development of inflammatory diseases such as endometriosis include the cytokines. Previous studies from our laboratory have demonstrated that reciprocal communication occurs between macrophages/monocytes and endometrial stromal cells in cell culture [5] [6] These studies demonstrated that factors secreted by macrophages/monocytes caused differential gene expression in telomerase-immortalized human endometrial stromal cells (T-HESC) and vice-versa. In the current project we tested the hypothesis that specific cytokines and growth factors secreted by macrophages (tumor necrosis factor α (TNFα), interleukin 1β (IL1β), interleukin 6 (IL6), and interleukin 8 (IL8), and the growth factor, transforming growth factor β (TGFβ)) cause gene expression changes in T-HESC cells that reproduce the effects of macrophage conditioned medium. We tested whether TNFα and IL1β increased the migratory and invasive properties of T-HESC cells
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