PDF(Pubmed)
Abstract：
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 (n = 40). The cell line was derived from the endometrium of patients with extragenital endometriosis (n = 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.
摘要：
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。kisspeptin（KISS1）基因最初被发现是转移的抑制因子。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KISS1，其受体（KISS1R），有和没有子宫内膜异位症的女性在位和异位子宫内膜中的MMP-2和MMP-9。我们推测KISS1和MMPs的失调可能与子宫内膜异位症的发病有关。免疫荧光研究的样本是从I-IV期确诊为子宫内膜异位症的患者收集的，年龄23至38岁（n=40）。该细胞系来自性外子宫内膜异位症患者的子宫内膜（n=7）。KISS1和KISS1R表达存在于外型子宫内膜异位症患者异位内膜,与不表达这些蛋白质的对照组相反。在子宫内膜异位症的所有阶段，KISS1和KISS1R值均降低。MMP-2和MMP-9基因在II期表达有统计学意义的增加，III,和IV系外型子宫内膜异位症。MMP合成在子宫内膜异位症的最后阶段增加。我们推想KISS1/KISS1R体系将来可以作为克制复合物削减MMP-2和MMP-9的表达，防止子宫内膜细胞的侵袭。
