EVALUATION OF METHYLATION STATUS OF PROGESTERONE RECEPTOR GENE IN CASES WITH ENDOMETRIOSIS

Endometriosis represents a common gynecological disease which affects >10% of women of reproductive age. Endometriosis is the presence and growth of functional endometrial tissue, outside the uterine cavity, primarily in the ovaries, pelvic peritoneum and rectovaginal septum. The main pathological processes are peritoneal inflammation and fibrosis, and the formation of adhesions and ovarian cysts. Infertility and pelvic pain are the predominant symptoms. Epigenetics is the study of heritable changes in gene function that do not involve changes in the DNA sequence. Epigenetic mechanisms may play a significant role in the origin and progression of endometriosis. Epigenetics encompasses several different phenomena, such as DNA methylation, histone modifications, RNA interference and genomic imprinting. Progesterone induces the differentiation of endometrial stromal cells to decidualized cells and glandular epithelial cells to the secretory phenotype. Representative molecular markers of progesterone action include increased production of epithelial glycodelin and stromal prolactin in the endometrium. Progesterone resistance has been viewed as a general feature in endometriosis and can be attributed to the extremely low progesterone-receptor levels in endometriotic tissue.