Kleimenova Tatiana, Polyakova Victoria, Linkova Natalia, Drobintseva Anna, Medvedev Dmitriy, Krasichkov Alexander
Department of Medical Biology, Federal State Budgetary Educational Institution of Higher Education, St. Petersburg State Pediatric Medical University, Ministry of Healthcare of the Russian Federation, 194100 St. Petersburg, Russia.
Research Laboratory for the Development of Drug Delivery Systems, St. Petersburg State Research Institute of Phthisiopulmonology, Ministry of Healthcare of the Russian Federation, 2-4, Ligovskiy pr., 191036 St. Petersburg, Russia.
Biomedicines. 2024 Jan 1;12(1):94. doi: 10.3390/biomedicines12010094.
Endometriosis is characterized by a condition where endometrial tissue grows outside the uterine cavity. The mechanisms of endometrium growth during endometriosis might be similar to the development of a tumor. The kisspeptin (KISS1) gene was initially discovered as a suppressor of metastasis. Matrix metalloproteinases (MMPs) and their inhibitors are described as factors in the early stages of endometriosis and tumor growth progression. We applied the quantitative polymerase chain reaction and the immunofluorescence method to investigate KISS1, its receptor (KISS1R), MMP-2, and MMP-9 in the eutopic and ectopic endometrium in women with and without endometriosis. We presume that the dysregulation of KISS1 and MMPs might contribute to endometriosis pathogenesis. Samples for the immunofluorescence study were collected from patients with a confirmed diagnosis of endometriosis in stages I-IV, aged 23 to 38 years old ( = 40). The cell line was derived from the endometrium of patients with extragenital endometriosis ( = 7). KISS1 and KISS1R expression are present in the ectopic endometrium of patients with extragenital endometriosis, as opposed to the control group where these proteins were not expressed. There is a decrease in KISS1 and KISS1R values at all stages of endometriosis. MMP-2 and MMP-9 genes express statistically significant increases in stages II, III, and IV of extragenital endometriosis. MMP synthesis increased in the last stages of endometriosis. We suppose that the KISS1/KISS1R system can be used in the future as a suppressive complex to reduce MMP-2 and MMP-9 expression and prevent endometrial cells from invading.
子宫内膜异位症的特征是子宫内膜组织在子宫腔外生长。子宫内膜异位症期间子宫内膜生长的机制可能与肿瘤的发展相似。亲吻素(KISS1)基因最初被发现是一种转移抑制因子。基质金属蛋白酶(MMPs)及其抑制剂被描述为子宫内膜异位症和肿瘤生长进展早期阶段的因素。我们应用定量聚合酶链反应和免疫荧光方法研究了有或无子宫内膜异位症女性的在位和异位子宫内膜中的KISS1、其受体(KISS1R)、MMP-2和MMP-9。我们推测KISS1和MMPs的失调可能有助于子宫内膜异位症的发病机制。免疫荧光研究的样本取自确诊为I-IV期子宫内膜异位症的患者,年龄在23至38岁之间(n = 40)。细胞系来自生殖器外子宫内膜异位症患者的子宫内膜(n = 7)。与未表达这些蛋白质的对照组相反,生殖器外子宫内膜异位症患者的异位子宫内膜中存在KISS1和KISS1R表达。在子宫内膜异位症的所有阶段,KISS1和KISS1R值均降低。在生殖器外子宫内膜异位症的II、III和IV期,MMP-2和MMP-9基因表达有统计学意义的增加。在子宫内膜异位症的最后阶段,MMP合成增加。我们推测,KISS1/KISS1R系统未来可作为一种抑制复合物,以降低MMP-2和MMP-9的表达,并防止子宫内膜细胞侵袭。