Guan Yong-Mei, Carlberg Magdalena, Bruse Christine, Carlström Kjell, Bergqvist Agneta
Department of Clinical Sciences, Unit for Obstetrics and Gynecology, Huddinge University Hospital, Stockholm, Sweden.
Acta Obstet Gynecol Scand. 2002 May;81(5):389-97.
To investigate whether endometriotic stromal cells release the urokinase plasminogen activator, soluble urokinase plasminogen activator receptor and plasminogen activator inhibitor-1. If so, to establish if there are any differences between endometrial stromal cells from women with and without endometriosis, and whether the release is hormonally regulated.
Biopsies were obtained from endometriotic tissue and from endometrium from women with and without endometriosis. Stromal cells were isolated, incubated and treated with estradiol-17beta, progesterone or raloxifen. Incubation media collected at 0, 24, 48 and 72 h were analyzed by enzyme-linked immunosorbent assay.
All these types of stromal cells released the urokinase plasminogen activator, soluble urokinase plasminogen activator receptor and urokinase plasminogen inhibitor-1. There was a significantly higher release of urokinase plasminogen inhibitor-1 and lower release of urokinase plasminogen activator and soluble urokinase plasminogen activator receptor in endometriotic cells. The release of urokinase plasminogen activator from endometrial stromal cells decreased during the study period both in control cultures and in cultures treated with progesterone or estradiol-17beta, but not in cultures treated with raloxifen nor in endometriotic cultures. The given hormones did not influence the release of the soluble urokinase plasminogen activator receptor. Progesterone significantly increased the urokinase plasminogen inhibitor-1 release in endometrial cells from both patient categories, and raloxifen significantly reduced the urokinase plasminogen inhibitor-1 release from stromal cells from both tissue categories from endometriotic patients. Estradiol-17beta had no effect.
This study shows that stromal cells from endometrium and endometriotic tissues release the urokinase plasminogen activator, soluble urokinase plasminogen activator receptor and urokinase plasminogen inhibitor-1. The release is partly hormonally regulated, but differently in endometriotic than in endometrial cells.
研究子宫内膜异位症基质细胞是否释放尿激酶型纤溶酶原激活物、可溶性尿激酶型纤溶酶原激活物受体和纤溶酶原激活物抑制剂 -1。如果是,确定患有和未患有子宫内膜异位症的女性的子宫内膜基质细胞之间是否存在差异,以及这种释放是否受激素调节。
从患有和未患有子宫内膜异位症的女性的异位内膜组织和子宫内膜获取活检样本。分离基质细胞,进行培养并用17β - 雌二醇、孕酮或雷洛昔芬处理。在0、24、48和72小时收集的培养上清液通过酶联免疫吸附测定进行分析。
所有这些类型的基质细胞均释放尿激酶型纤溶酶原激活物、可溶性尿激酶型纤溶酶原激活物受体和尿激酶型纤溶酶原抑制剂 -1。子宫内膜异位症细胞中尿激酶型纤溶酶原抑制剂 -1的释放显著更高,而尿激酶型纤溶酶原激活物和可溶性尿激酶型纤溶酶原激活物受体的释放更低。在研究期间,对照培养物以及用孕酮或17β - 雌二醇处理的培养物中,子宫内膜基质细胞的尿激酶型纤溶酶原激活物释放均减少,但在用雷洛昔芬处理的培养物以及子宫内膜异位症培养物中未减少。所给予的激素不影响可溶性尿激酶型纤溶酶原激活物受体的释放。孕酮显著增加了两类患者子宫内膜细胞中尿激酶型纤溶酶原抑制剂 -1的释放,雷洛昔芬显著降低了子宫内膜异位症患者两类组织的基质细胞中尿激酶型纤溶酶原抑制剂 -1的释放。17β - 雌二醇无作用。
本研究表明,子宫内膜和子宫内膜异位症组织的基质细胞释放尿激酶型纤溶酶原激活物、可溶性尿激酶型纤溶酶原激活物受体和尿激酶型纤溶酶原抑制剂 -1。这种释放部分受激素调节,但在子宫内膜异位症细胞和子宫内膜细胞中的调节方式不同。