Heparanase And Metastin Express In Adenomyosis And The Influence Of Mifepristone For Their Expression And Significance

Bachground Adenomyosis (AM), that is endometrial myometrial invasion more than up to a high power field, pathological diagnosis of endometrial glands and stroma appears at next the endometrial basal layer of the≥3mm. The etiology and pathogenesis is unclear, may be related to mechanical factors, endocrine factors, apoptosis factors, immune factors, and so on. With the progress of the study, many academics believe that the occurrence of adenomyosis have related to endometrial glands and stroma having invasiveness.Heparanase (Hpa) as a glucuronic acid esterase, by cracking acetyl heparan sulphate proteoglycans, release and activation of vascular endothelial growth factor (VEGF), basic fibroblast growth factor, promote cell growth and transfer, while mediated cell adhesion, in extracellular matrix cell-cell contact, growth and differentiation process play an important role,involved in a series of physiological and pathological processes.Metastin is protein encodes from Kiss-1 gene, the protein mainly through acting on their receptors to regulate calcium levels, so that increase in the concentration of calcium ions to suppress the invasive cell chemotaxis, proliferation and transfer to play inhibit metastasis of tumor cells.Mifepristone is a progesterone receptor (PR) antagonist, can reduce endometrial angiogenesis, make endometrial spiral arteries to shrink, uterine blood flow decreased and endometrial thinned so that take endometrium anti-proliferative effect.This topic was designed to detect the HPA, metastin expression in adenomyosis in vitro eutopic endometrial glandular epithelial cells and the effects of mifepristone on their expression,to explore the pathogenesis of adenomyosis in the presence of invasive factors, if Mifepristone could intervent these factors with its possible mechanisms of intervention..Objective Detection the expression of HPA and metastin in adenomyosis in vitro eutopic endometrial glandular epithelial cells and in the control group of endometrial glandular epithelial cells and the effects of mifepristone on the two kinds of protein expression in case group, to understand the pathogenesis of adenomyosis that may exist in aggressive factors and to explore the interfere mechanism of mifepristone to factors.Methods Culturing in vitro Adenomyosis eutopic endometrial glandular epithelial cells and the control group (uterine fibroids group) endometrial glandular epithelial cells, and some of cases groups cells cultured with mifepristone intervention (in each group according to proliferative phase, distinguish secretory phase culture). By western-blot detect quantitatively of HPA and the metastin in the adenomyosis group, drug intervention group and the control group (uterine fibroids group) cultured cells. Using statistical analysis of the two indicators in each group expression differences.Results (1) HPA expressed in adenomyosis group higher than control group both at proliferative phase and secretory phase eutopic endometrial glandular epithelial cells (p<0.05), metastin expression lower than the control group (p<0.05). (2) adenomyosis group of proliferative phase and secretory phase cells were for drug intervention, HPA expression reduced, metastin expression increased,as compared with non-medication group the difference was statistically significant (p<0.05). (3) group of cells in adenomyosis HPA and metastin expression in proliferative phase and secretory phase was not statistically significant when compared (p> 0.05)Conclusion Expression imbalance of invasive factors and invasive inhibiting factor in endometrial glandular cells may be one of pathogenesis of adenomyosis, intervention of mifepristone on the HPA and metastin may be one of the mechanisms that Mifepristone inhibit the development of adenomyosis...