Results
| PMID | 19260858 |
| Gene Name | TNF |
| Condition | Endometriosis |
| Association |
Associated |
| Sex | Female |
| Associated genes | cIAP2, IL-8, NFkappaB, TNFalpha |
| Other associated phenotypes |
Endometriosis |
|
Am J Reprod Immunol. 2009 Apr;61(4):277-85. doi: Miyamoto, Ayako| Taniguchi, Fuminori| Tagashira, Yukiko| Watanabe, Ayako| Harada, Tasuku| Terakawa, Naoki Department of Obstetrics and Gynecology, Tottori University School of Medicine, Nishimachi, Yonago, Japan. PROBLEM: We previously reported that lipopolysaccharide (LPS)-promoted endometriotic stromal cell (ESC) proliferation by inducing TNFalpha production. The aim of this study was to investigate the efficacy of TNFalpha gene silencing on LPS-treated ESCs. METHOD OF STUDY: Endometriotic stromal cells (ESCs) and endometrial stromal cells (ESCs) (EMSCs) were obtained from ovarian chocolate cysts and uterine myoma, respectively. Using PCR array, LPS-induced gene expression profiling after transfection of TNFalpha siRNA into ESCs was performed. Down-regulated genes by TNFalpha silencing were examined using real-time RT-PCR. Effect of TNFalpha silencing was examined using ELISA and BrdU incorporation, respectively. RESULTS: In PCR array, TNFalpha silencing in ESCs repressed LPS-induced expression of cIAP2 and IL-8, NFkappaB pathway responsive genes. After adding LPS, the levels of cIAP2 and IL-8 expression in ESCs were higher compared with those in EMSCs. TNFalpha silencing attenuated the LPS-induced ESC proliferation. CONCLUSION: Tumor necrosis factor alpha may be involved in cell proliferation of endometriotic tissues. Mesh Terms: Apoptosis/immunology| Cell Proliferation/drug effects| Cells, Cultured| Endometriosis/genetics/*immunology/pathology| Endometrium/pathology| Female| Gene Expression Profiling| Gene Silencing| Humans| Inhibitor of Apoptosis Proteins/genetics/immun |
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