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  • Title: Reduced endothelial cell migratory signal production by endometrial explants from women using Norplant contraception.
    Author: Subakir SB, Hadisaputra W, Siregar B, Irawati D, Santoso DI, Cornain S, Affandi B.
    Journal: Hum Reprod; 1995 Oct; 10(10):2579-83. PubMed ID: 8567774.
    Abstract:
    Bleeding problems can be one of the major reasons for women to discontinue the use of hormonal contraceptives. Causes of endometrial bleeding can include disturbances in endometrial regeneration and angiogenesis. Endothelial cells migrate and proliferate rapidly as part of the angiogenic process under the influence of appropriate stimuli. The aim of this study is to investigate the production of endothelial cell migratory signals by endometrial explants from women receiving Norplant and to compare it to that of those with a normal menstrual cycle. The subjects were selected from Norplant users with an exposure of 3-9 months. The endothelial cell migratory signal production was assayed using the Folkman method (1989), modified by Rogers (1992). Blood serum concentrations of oestradiol, progesterone and sex hormone binding globulin were monitored for 2 weeks prior to endometrial biopsy. Endothelial cell migration toward endometrial explants of 30 women as control and 46 Norplant acceptors was assayed. The results showed that endothelial cell migratory activity toward endometrial explants from the control group was significantly higher than toward those from Norplant acceptors (z = 3.89, P < 0.001). There were no differences between endometrial endothelial cell migratory activities in Norplant acceptors with bleeding or without bleeding problems. Researchers examined the production of endothelial cell migratory signals by endometrial explants from 46 Norplant acceptors aged 18-40 and compared it with endothelial cell migratory signals produced by endometrial explants from women using no hormonal contraception or an IUD and having a normal menstrual cycle. The results will provide insight into the role of endothelial cell migration in endometrial bleeding among Norplant acceptors. Both cases and controls attended the Raden Saleh Clinic in Jakarta, Indonesia. Health providers took peripheral blood samples 6 times at 2-3 day intervals before the endometrial biopsy to monitor serum levels of estradiol, progesterone, and sex hormone-binding globulin (SHBG). Laboratory researchers used a three-dimensional collagen matrix culture medium containing dispersed human umbilical vein endothelial cells as modified by Rogers (1992) to conduct the endothelial cell migration assay. Endothelial cell migration toward endometrial explants of the control group was much higher than toward those of the Norplant group (p 0.001). For example, 30 of 46 of the Norplant endometrial explants had a median endothelial cell migratory score of zero compared to 8 of the 30 control biopsies. In fact, only 1 of the control biopsies of the individual 500-cubic-micrometer explants did not respond, while 19 of the like Norplant explants did. In controls, endothelial cell migration was greater in the proliferative phase than in the secretory phases. Endothelial cell migration toward endometrial biopsies of Norplant acceptors with bleeding problems was the same as that toward Norplant acceptors with no bleeding problems. Serum levels of estradiol, progesterone, and SHBG were not associated with endothelial cell migration. These findings do not support the belief that increased angiogenesis in the endometrium of Norplant acceptors is responsible for endometrial bleeding.
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