Induction of endometrial epithelial cell invasion and c-fms expression by transforming growth factor beta.
Induction of endometrial epithelial cell invasion and c-fms expression by transforming growth factor beta.
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DOI：
10.1093/molehr/gap043
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发表时间：
2009-10
影响因子：
4
通讯作者：
Ya‐Guang Liu;R. Tekmal;P. Binkley;H. Nair;R. Schenken;N. Kirma
中科院分区：
文献类型：
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作者：
Ya‐Guang Liu;R. Tekmal;P. Binkley;H. Nair;R. Schenken;N. Kirma
子宫内膜异位症患者腹腔液中转化生长因子β 1（TGF-β 1）水平升高，子宫内膜细胞表达TGF-β信号成分;然而，关于TGF-β在子宫内膜异位症中的作用知之甚少。我们的目的是研究TGF-β 1对（i）由c-fms基因编码的巨噬细胞集落刺激因子受体的表达，（ii）子宫内膜细胞的transmesothelium侵袭性，（iii）细胞增殖和（iv）附着于腹膜间皮细胞（PMC）的影响。通过实时荧光定量RT-PCR和流式细胞术测定TGF-β 1对c-fms mRNA表达的影响。利用三维体外腹膜模型系统研究了TGF-β 1对永生化子宫内膜上皮细胞（EEC）系EM 42和原代EEC侵袭力的影响。还使用已建立的技术检查了细胞增殖和与PMC的附着。TGF-β 1对细胞增殖和子宫内膜细胞与PMC的粘附几乎没有影响。TGF-β 1显著诱导c-fms mRNA表达和c-fms细胞表面表达。TGF-β 1增强EM 42细胞和EECs的跨间皮侵袭。TGF-β 1信号的拮抗剂显著抑制c-fms表达和细胞侵袭的诱导，这表明有必要进行额外的研究来评估TGF-β拮抗剂在子宫内膜异位症中的治疗潜力。
Transforming growth factor beta 1 (TGF-beta1) levels are increased in the peritoneal fluid of endometriosis patients, and endometrial cells express TGF-beta signaling components; however, little is known regarding the role of TGF-beta in endometriosis. Our objective was to examine the effects of TGF-beta1 on (i) the expression of macrophage colony-stimulating factor receptor encoded by the c-fms gene, (ii) transmesothelial invasiveness of endometrial cells, (iii) cellular proliferation and (iv) attachment to peritoneal mesothelial cells (PMCs). Effects of TGF-beta1 on c-fms mRNA expression were determined by real-time RT-PCR and c-fms cell-surface expression by flow cytometry. Effects of TGF-beta1 on the invasiveness of the immortalized endometrial epithelial cell (EEC) line EM42 and primary EECs were examined using a three-dimensional in vitro system modeling the peritoneum. Cellular proliferation and attachment to PMCs were also examined using established techniques. TGF-beta1 had little or no effect on cellular proliferation and endometrial cell attachment to PMCs. TGF-beta1 significantly induced the expression of c-fms mRNA and c-fms cell-surface expression. TGF-beta1 enhanced transmesothelial invasion by EM42 cells and EECs. Antagonists of TGF-beta1 signaling significantly inhibited both the induction of c-fms expression and cellular invasiveness, suggesting that additional studies are warranted to assess the therapeutic potential of TGF-beta antagonists in endometriosis.