P-189: Investigation of Vascular Endothelial Growth Factor Receptors Expression in Ectopic Pregnancy
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Abstract:
Background: Ectopic pregnancy (EP) is a complication of conception in which the embryo implants outside of uterine cavity. The increasing incidence of serious maternal morbidity resulting from EP has prompted the search for biomarkers to aid in early diagnosis and take advantage of conservative treatments. One of the effective biomarkers in EP is vascular endothelial growth factor (VEGF). VEGF is an angiogenic growth factor that has an important role in regulating trophoblast functions in the process of placentation and implantation. This molecule acts on endothelial cells through their receptors flt-1 (VEGFR1) and fkl-1/KDR (VEGFR2) to exert their effects. VEGFR-2 mediates almost all of the known cellular responses to VEGF. VEGFR-1 modulates VEGFR- 2 signaling. The purpose of our study is to determine levels of VEGFR1 and VEGFR2 in fallopian tubes (FTs) carrying EP. Materials and Methods: In this study, biopsies from Infundibulum, Ampulla and Isthmus of FTs were obtained from case and control groups. Case and control groups were women who underwent salpingectomy for EP and hysterectomy respectively. Human chorionic gonadotropin (hCG) was injected in 14 days leading up to hysterectomy to produce a state of pseudo-pregnancy. In this investigation expression of VEGFR1-2 were tested with RT-PCR. Also Q-PCR was used to compare quantitative expression of these receptors between two groups.Results: RT-PCR has shown expression of VEGFR1-2 in infundibulum, Ampulla and Isthmus from case and control groups. Q-PCR has shown, variable expression of VEGFR1-2 in all parts of FTs carrying EP compared with control group. Conclusion: Hypoxia plays important role in the regulation of VEGFR1-2 expression. It is possible that implantation in the tubal ectopic environment associated with increasing of hypoxia. This may lead to variation of VEGFR1-2 expression in FTs carrying EP compared with control group.
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volume 6 issue 2
pages -
publication date 2012-09-01
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