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Effect of Growth Hormone on the Thickness of Proliferative Endometrium and the Expression of VEGF, EGF, IGF-I in Mouse

Author: ZhangJie
Tutor: TanLi
School: Zhengzhou University
Course: Obstetrics and Gynaecology
Keywords: Growth Hormone Endometrial Growth factor Endometrial receptivity
CLC: R714.8
Type: Master's thesis
Year: 2007
Downloads: 251
Quote: 1
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Abstract

Background and purpose in recent years due to the impact of social and environmental factors, the incidence of infertility increased gradually from assisted reproductive technology (Assisted reproductive technology, ART) has been widely carried out. Assisted reproductive technology, clinical pregnancy rate has been hovering at a low level. One important factor i.e. reduce endometrial receptivity (uterine receptivity) within the key to a very short period only in the normal state of the endometrial receptivity embryos capacity (i.e. the endometrial receptivity) , usually in the menstrual cycle of 20 to 24d after the LH peak in the first 7 to 11d. The endometrial show blastocysts growing receptivity. Gland increases bending, the glandular cavity contains a lot of mucus and glycogen, endometrial vascular congestion, conversion of stromal cells to decidual cells and changes in embryonic development synchronized, so that the pro-embryo adhesion and implantation. In addition, clinical endometrium is too thin (<7mm) patients pregnancy rate is also lower bound to affect the receptivity of the secretory phase, proliferative endometrium is too thin. Clinically, these patients, how to improve their endometrial thickness is still not recognized, the effect of certain therapies. Present study found that a variety of factors can affect the adhesion of endometrial receptivity and trophoblast, the endometrial estrogen and progesterone (E ₂ P) role in the secretion of a variety of cell cytokines and adhesion molecules, through endocrine, paracrine regulator of endometrial receptivity embryo implantation by steroid hormones - immune cells - cytokines, adhesion molecules network. A variety of regulatory molecules involved in the process of embryo implantation, such as leukemia inhibitory factor (leukemia inhibitory factor, LIF) integrin family (integrins are), pinopodes calcitonin, vascular endothelial growth factor (vascular endothelial growth factor, VEGF) Epidermal growth factor (epidermal growth factor, EGF), insulin-like growth factor (insulin-like growth factor, IGFs), etc.. Vascular endothelial growth factor (VEGF) is the original and has a specific angiogenic endothelial cell mitogen vascular permeability, vascular endothelial cell division, proliferation, induction of angiogenesis. In recent years, vascular endothelial growth factor (VEGF) plays an important role in uterine angiogenesis process. Both early proliferation of endometrial repair or suffer the implantation of the embryo in mid-secretory have higher expression of VEGF in the endometrium. Angiogenesis is undoubtedly the most active in the process of embryo implantation endometrium, and maternal blood contact. Increased around the bed of VEGF, may contribute to endometrial receptivity, in order to facilitate the formation of embryo implantation and early villous vessels, lack of VEGF, the uterus receptivity decline, villi form bad. Epidermal growth factor (EGF) exists in each of endometrial cells in the menstrual cycle the proliferative phase EGFmRNA level is low, protein expression in endometrial cell growth and differentiation regulation autocrine and paracrine factor cavity epithelial cells and stromal cells, glandular epithelial cells did not express, and then gradually steady increase in the secretion of the window of implantation (19 to 21 days), the highest expression, and positioning in most surface to secrete interim luminal epithelial cells, EGF regulating the proliferation of endometrial epithelial cells and stromal cells, by expression in endometrial vivo E ₂ P regulation, with the embryo implantation site endometrium EGF high expression, EGF plays an important role in embryo implantation. Insulin-like growth factors (IGFs) is a multifunctional growth factors, play an important role on cell proliferation, differentiation and metabolism. Of IGFs in normal menstrual cycle of IGFs receptors and their binding proteins in endometrial expression of varying degrees, their main source of secretory endometrium. IGF-Ⅰ and IGF-Ⅱ mitogen role in local play, can also induce cell differentiation. Major gene and mRNA expression of IGF-Ⅰ gene and mRNA in the proliferative phase and early secretory endometrium, IGF-Ⅱ and Ⅰ type II IGF receptor mRNA is expressed mainly in secretory endometrium and early pregnancy decidua. Time and cell-specific expression, suggesting that IGFs may be associated with cyclical changes in endometrial receptivity. Growth hormone (growth hormone, GH) is a peptide hormone of pituitary secretion, clinical application of growth hormone auxiliary ovulation induction may enhance ovarian gonadotropin (gonadotropin, Gn) sensitivity, reduce human menopausal gonadotropin the amount of the hormone (HMG), improve the function of the ovaries, indirect regulation of follicular development, improve the the follicles quality and get more mature eggs. The study showed that: The uterus also GH synthesis and the role of a non-pituitary sites, and to the paracrine and autocrine regulation of reproductive function. Sheep, GH uterine milk protein mRNA levels and the number of uterine layer cavernous glands to increase the number of endometrial and uterine pregnancy. Sbracia M and other recent study found that the growth hormone receptor in human and mouse endometrium, strong expression and secretion in advanced endometrial glandular cells and early pregnancy decidua that growth hormone plays a very important in embryo implantation role. In this study, experimental animals mice as a model, to observe growth hormone mice proestrus namely proliferative phase endometrial thickness and proliferative phase endometrium, the luminal epithelium and stroma of VEGF, EGF, IGF-Ⅰ expression explore the impact of GH endometrial microenvironment and the estimated the GH endometrial thickness and endometrial receptivity impact, providing a theoretical basis for assisted reproductive technology, clinical medicine. MATERIALS AND METHODS Experimental animals were purchased from the Experimental Animal Center of Zhengzhou University, 50 female mice were randomly divided into two groups. Experimental group for the injection of growth hormone (GH) group, the control group was injected with saline (NS) group. Immunohistochemical SP method detect endometrial VEGF, EGF, IGF-I expression multifunctional image analyzer to measure the thickness of the lining of the uterus. Experimental data application SPSS11.5 statistical package handling, measurement data are presented as mean ± standard deviation ((?) ± s) using ANOVA analysis determines differences between the two groups of data using two sample t-test, a = 0.05 significant test level. Results 1. The GH group endometrial thickness of 412.86 ± 0.70μm, the control group was 381.27 ± 0.35μm, and the difference was statistically significant (P <0.05). 2. Parts of the same for the two groups of VEGF, EGF, IGF-I expression. 3. VEGF expression in endometrial epithelial cytoplasm, cell membrane, weak expression of interstitial; the GH of VEGF in endometrial glandular epithelial cytoplasmic membrane, gland expression intensity was significantly higher than the two groups the difference was statistically significant (P <0.05), compared to VEGF expression in stromal two groups showed no significant sex (P> 0.05). 4. EGF is mainly expressed in endometrial glandular epithelium, glandular, stromal cells have a moderate amount of expression; the GH groups EGF expression was significantly higher than that in the control group, two groups the difference was statistically significant (P <0.05). 5. IGF-Ⅰ expression in mouse endometrial stromal cells, glandular weak expression in the glandular epithelium. Strength of the GH group IGF-Ⅰ expression in stromal cells was significantly higher than that in the control group, the two groups compared the difference was statistically significant (P <0.05), but no statistically compared to the expression of the two groups in the glandular epithelium, glandular significance (P> 0.05). Conclusion 1. Growth hormone can improve mouse endometrium thickness prompt growth hormone may endometrial glands hyperplasia, interstitial differentiation, play an important role. 2. Growth hormone can promote endometrial growth factor: of VEGF, EGF, IGF-Ⅰ expression, and thereby improve the endometrial microenvironment. 3. VEGF, EGF, IGF-Ⅰ common expression in the endometrium, the possible interactions between them, mutual restraint to the regulation of biochemical changes in the endometrium. 4. Growth hormone in the mouse endometrium series of changes, growth hormones play a role in improving endometrial receptivity.

Effect of Growth Hormone on the Thickness of Proliferative Endometrium and the Expression of VEGF, EGF, IGF-I in Mouse

Abstract

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