Regulation of FAS Ligand Expression by Chemokine Ligand 2 in Human Endometrial Cells

Belgin Selam, Umit A Kayisli, G Eda Akbas, Murat Basar, Murat Başar, Aydin Arici, Aydın Arıcı
Biology of reproduction · 2006 · vol. 75(2) , pp. 203–209 · doi:10.1095/biolreprod.105.045716 · W2111290643
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Chemokine ligand 2 (CCL2) upregulates Fas ligand protein expression in human endometrial stromal cells, leading to increased Jurkat cell apoptosis when cocultured, suggesting a mechanism for local immunotolerance in endometriosis.

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Abstract

Human endometrium is a dynamic tissue under the influence of numerous hormones, growth factors, and cytokines interacting to maintain a balance of cellular growth, differentiation, and apoptosis. We have previously demonstrated that several factors including interleukin-8, extracellular matrix, and steroid hormones modulate FASLG, one of the apoptotic molecules, in human endometrium. Chemokine ligand 2 (CCL2), a monocyte chemoattractant and activating factor, is a cytokine involved in endometrial function. CCL2 is elevated in the peritoneal fluid of women with endometriosis. We hypothesize that increased levels of CCL2 in the endometriotic environment may upregulate FASLG expression in human endometrial stromal cells and induce a local immunotolerance in endometriosis. To test our hypothesis, we studied the in vitro regulation of FASLG expression and apoptosis by CCL2 in endometrial stromal cells. Western blot analysis revealed that CCL2 upregulated FASLG protein expression in cultured endometrial stromal cells. Based on semiquantitative RT-PCR analysis, CCL2 did not alter either FAS or FASLG mRNA expression in endometrial stromal cells. Immunocytochemistry results from the same cells treated with CCL2 demonstrated upregulation of FASLG protein expression. CCL2 did not change rate of apoptosis in endometrial stromal cells as evaluated by TUNEL assay. However, an increased apoptotic rate was detected in Jurkat (T lymphocytes) cells cocultured with endometrial stromal cells previously treated with CCL2. We speculate that increased FASLG expression by CCL2 may induce apoptosis of T lymphocytes and thus produce an immunotolerant environment for the development of ectopic implants.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Chemokine CCL2 Endometrium Endometrium Fas Ligand Protein Adult Apoptosis Apoptosis Cells, Cultured Chemokine CCL2 Chemokine CCL2 Endometriosis Endometriosis Endometriosis Endometrium Endometrium Fas Ligand Protein Fas Ligand Protein fas Receptor fas Receptor fas Receptor

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