کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2775190 1152314 2012 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Re-establishment of gap junctional intercellular communication (GJIC) between human endometrial carcinomas by prostaglandin E2
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیوشیمی بالینی
پیش نمایش صفحه اول مقاله
Re-establishment of gap junctional intercellular communication (GJIC) between human endometrial carcinomas by prostaglandin E2
چکیده انگلیسی

Reduced intercellular communication via gap junctions is correlated with carcinogenesis. Gap junctional intercellular communication (GJIC), between normal human endometrial epithelial cells is enhanced when endometrial stromal cells were present in culture. This enhancement of GJIC between normal epithelial cells also occurs when they are cultured in medium conditioned by stromal cells. This observation indicated that a soluble compound (or compounds) produced and secreted by stromal cells mediates GJIC in epithelial cells. Previous studies have shown that endometrial stromal cells release prostaglandin E2 (PGE2) and prostaglandin F2α (PGF2α) under physiological conditions. When we evaluated the response of normal endometrial epithelial cells to various concentrations of PGE2, we found enhanced GJIC with 1 nM PGE2. This is a smaller increase in GJIC than that induced by medium conditioned by stromal cells. When the extracellular concentration of PGE2 was measured after incubation with stromal cells, it was found to be similar to the concentrations showing maximal GJIC between the normal epithelial cells. When indomethacin was used to inhibit prostaglandin synthesis by stromal cells, GJIC was reduced but not eliminated between normal endometrial epithelial cells. These observations suggest that although PGE2 secreted by stromal cells is an important mediator of GJIC between the epithelial cells, it is not the sole mediator. Transformed endometrial epithelial cells did not demonstrate GJIC even in the presence of stromal cells. However, we were able to re-establish GJIC in transformed epithelial cells when we added PGE2 to the cells. Our findings show that PGE2 may serve as an intercellular mediator between stromal and epithelial cells that regulates GJIC in normal and malignant epithelial cells. This suggests that maintenance of GJIC by preserving or replacing PGE2 secretion by endometrial stromal cells may have the potential to suppress carcinogenesis in endometrial epithelial cells.


► Endometrial epithelial-stromal cell co-cultures mimic endometrial tissue functions.
► Stromal cells in co-cultures activate GJIC between normal epithelial cells.
► Medium conditioned by stromal cells activate GJIC in normal epithelial cells.
► Prostaglandin E2 in medium induces GJIC activity between normal epithelial cells.
► Prostaglandin E2 restores some GJIC activity between endometrial cancer cells.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental and Molecular Pathology - Volume 93, Issue 3, December 2012, Pages 441–448
نویسندگان
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