Hypothesis/aims of study. Kisspeptin (KISS1) is encoded by KISS1 gene and its interaction with KISS1 receptor (KISS1R) suppresses metastasis and regulates release of gonadotropin-releasing hormone, which promotes secretion of estradiol and progesterone. Steroid hormone synthesis is regulated by KISS1/KISS1R and its activation can be involved in hormone dependent disorders such as endometriosis. KISS1 expression has been shown to inhibit the activity of a number of matrix metalloproteinases (MMPs). In this study, we aimed to isolate endometrial cell cultures from patients with and without endometriosis; to evaluate KISS1, KISS1R, MMP-2, and MMP-9 protein expression by immunocytochemistry; and to perform culture tests: the scratch assay and the analysis of cell migration activity. Results. It was found that the endometrial cell cultures expressed KISS1, KISS1R, MMP-2, and MMP-9 proteins, with the cell migration ability enhanced.
Hypothesis/aims of study. Melatonin is found in almost all living organisms, the range of its effects being quite diverse. Effects of this hormone in the human body are realized via two ways, through specific receptors and non-receptor pathways. Melatonin may act through both membrane and nuclear receptors. In the present work, the expression of MTR1 and MTR2 melatonin receptors was studied in the eutopic endometrium and endometrioid heterotopies, and the level of melatonin metabolite, 6-sulfatoxymelatonin, in daily urine in patients with genital endometriosis (GE) was analyzed. Study design, materials and methods. The experimental group included 67 patients of reproductive age with a verified diagnosis of GE, and the control group consisted of 18 individuals with an ovulatory menstrual cycle without gynecological pathology. The 6-sulfatoxymelatonin level in daily urine was determined by enzyme immunoassay. The study of MTR1 and MTR2 melatonin receptor expression in the endometrium and endometrioid heterotopies was performed in 24 patients with GE and in 10 women of reproductive age who were examined for infertility who did not have gynecological pathology based on diagnostic laparoscopy. To study the expression of melatonin receptors, the endometrium and endometrial heterotopy sampling was carried out from day 18 to day 22 of the menstrual cycle. Morphological assessment included histological and immunofluorescence studies using confocal laser scanning microscopy. Results. In patients with GE, there was found a tendency to a decrease in 6-sulfatoxymelatonin excretion in daily urine compared to the control group. It was also found that the total relative expression area of melatonin receptors in the endometrium of women with GE was significantly lower compared to the endometrium of patients from the control group. Significant differences between the average brightness and optical density were not found. In addition, it was revealed that the relative expression areas of MTR1 and MTR2 melatonin receptors in the eutopic endometrium and in endometrioid heterotopies did not differ significantly. A negative correlation was stated between the relative expression area of melatonin receptors and GE prevalence. Particular attention is paid to the role of melatonin in the development of GE and to the possibilities of working out new treatment regimens with its use. Conclusion. The data obtained confirm the undoubted role of melatonin in the pathogenesis of GE, however, the development of new treatment regimens with its use requires further study.
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