摘要：Embryo implantation is a complicated process involving mother and conceptus cells differentiation, proliferation and invasion that are essential for successful pregnancy. Almost every cell in the human body is affected by IGF-1 that is one of the most potent natural activators of cell growth and multiplication, and also a potent inhibitor of the programmed cell death. bFGF, acting via its receptor FGFR1, is one of the factors involved in mediating the angiogenesis, proteolysis and apoptosis during the implantation. OBJECTIVE: To establish pregnancy inducted difference of appearance of bFGF, IGF-1 and their receptors in the embryonic, decidual and tubal tissue. STUDY DESIGN: In this study 14 tubal pregnancy and 10 decidual tissue samples were evaluated immunohistochemically in order to define the distribution of bFGF, FGFR1, IGF-1, IGF-1R. RESULTS: The Mann-Whitney U test was used as appropriate for the evaluation of significant differences. FGFR1 appearance dominated on bFGF in the decidual (z=2.539, p=0.01), tubal (z=2.539, p=0.01) and embryonic (z=2.539, p=0.01) tissue. IGF-1 and IGF-1R appearance in the decidual, tubal and embryonic tissue was not statistically different. It was the same as IGF-1 and IGF-1R expression in gravid endometrium, but in the ectopic implantation site IGF-1R was particularly absent (z=1.935, p=0.05), only mesothelium and some epithelial cells stained. CONCLUSION: IGF-1, IGF-1R, bFGF and FGFR1 are widely appearing growth factors in actively developing and differentiating of the human embryonic tissue during the first trimester. Both endometrial and fallopian tube tissues express more FGFR1 than bFGF that testify the stimulation of compensatory adaptation of the organ during pregnancy. IGF-1 and IGF-1R richly appear in gravid endometrium. IGF-1 is widely distributed in both the mother and the embryo tissues but only some of them are IGF-1R marked in a case of ectopic pregnancy. The deficit of IGF-1R in the fallopian tube might bea result of cell growth restriction and the impaired process of trophoblast invasion.
