摘要
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.
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.
