Peroxisome-proliferator activator receptor-gamma activation decreases attachment of endometrial cells to peritoneal mesothelial cells in an in vitro model of the early endometriotic lesion.
Peroxisome-proliferator activator receptor-gamma activation decreases attachment of endometrial cells to peritoneal mesothelial cells in an in vitro model of the early endometriotic lesion.
复制标题
在早期子宫内膜异位病变的体外模型中，过氧化物酶体增殖物激活剂受体-γ激活降低了子宫内膜细胞与腹膜间皮细胞的附着。
DOI：
10.1093/molehr/gap061
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发表时间：
2009
影响因子：
4
通讯作者：
Lebovic,DI
中科院分区：
文献类型：
--
作者：
Kavoussi,SK;Witz,CA;Binkley,PA;Nair,AS;Lebovic,DI
本研究的目的是探讨过氧化物酶体增殖物激活受体（peroxisome proliferator-activated receptor，PPAR）-γ激活是否对早期子宫内膜病变的体外模型中子宫内膜细胞与腹膜间皮细胞的附着有影响。子宫内膜上皮细胞系EM 42和间皮细胞系LP 9用于本研究。用不同浓度（10、20和40 µM）的PPAR-γ激动剂环格列酮（CTZ）处理EM 42细胞、LP 9细胞或两者× 48 h，随后共培养EM 42和LP 9细胞。然后评估EM 42附着和侵袭通过LP 9细胞的速率，并与对照（EM 42和LP 9细胞共培养而没有预先用CTZ处理）进行比较。接下来，评估CTZ处理和未处理的EM 42细胞与透明质酸（HA）（腹膜间皮细胞上的细胞粘附分子（CAM））的附着。虽然当单独用CTZ处理LP 9细胞时，EM 42附着没有差异，但用40 μM CTZ处理EM 42细胞使EM 42与LP 9细胞的附着降低了27%（P< 0.01）。用40 μM CTZ处理EM 42和LP 9细胞，使EM 42与LP 9的附着减少37%（P< 0.01）。用40 μM CTZ处理EM 42细胞使其与HA的粘附降低了66%（P= 0.056）。CTZ并不降低EM 42细胞通过LP 9单层的侵袭。CTZ可抑制EM 42细胞增殖。总之，CTZ显着降低EM 42附着到LP 9细胞和HA在体外模型的早期乳腺癌病变。
The aim of this study was to investigate whether peroxisome proliferator-activated receptor (PPAR)-γ activation has an effect on the attachment of endometrial cells to peritoneal mesothelial cells in a well-establishedin vitromodel of the early endometriotic lesion. The endometrial epithelial cell line EM42 and mesothelial cell line LP9 were used for this study. EM42 cells, LP9 cells or both were treated with the PPAR-γ agonist ciglitazone (CTZ) at varying concentrations (10, 20 and 40 µM) × 48 h with subsequent co-culture of EM42 and LP9 cells. The rate of EM42 attachment and invasion through LP9 cells was then assessed and compared with control (EM42 and LP9 cells co-cultured without prior treatment with CTZ). Next, attachment of CTZ-treated and untreated EM42 cells to hyaluronic acid (HA), a cell adhesion molecule (CAM) on peritoneal mesothelial cells, were assessed. Although there was no difference in EM42 attachment when LP9 cells alone were treated with CTZ, treatment of EM42 cells with 40 µM CTZ decreased EM42 attachment to LP9 cells by 27% (P< 0.01). Treatment of both EM42 and LP9 cells with 40 µM CTZ decreased EM42 attachment to LP9 by 37% (P< 0.01). Treatment of EM42 cells with 40 µM CTZ decreased attachment to HA by 66% (P= 0.056). CTZ did not decrease invasion of EM42 cells through the LP9 monolayer. CTZ may inhibit EM42 cell proliferation. In conclusion, CTZ significantly decreased EM42 attachment to LP9 cells and HA in anin vitromodel of the early endometriotic lesion.