Immunoreactivity of Kisspeptin and Kisspeptin Receptor in Eutopic and Ectopic Endometrial Tissue of Women With and Without Endometriosis
Immunoreactivity of Kisspeptin and Kisspeptin Receptor in Eutopic and Ectopic Endometrial Tissue of Women With and Without Endometriosis
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DOI：
10.1007/s43032-020-00167-w
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发表时间：
2020-02-18
影响因子：
2.9
通讯作者：
Bedaiwy, Mohamed A.
中科院分区：
文献类型：
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作者：
Abdelkareem, Amr O.;Alotaibi, Fahad T.;Bedaiwy, Mohamed A.
子宫内膜异位症的特征是异位子宫内膜组织的存在。子宫内膜异位症的组织播散机制可能与肿瘤转移相似。我们假设子宫内膜癌转移抑制因子 Kisspeptin (KISS1) 的失调可能导致子宫内膜异位症的发病机制。在这项研究中，我们表征了患有和不患有子宫内膜异位症的女性在增殖期和分泌性月经周期阶段的在位和异位子宫内膜组织中 Kisspeptin 及其受体 KISS1R 的免疫反应性。使用 KISS1 和 KISS1R 抗体对患有 (n = 35) 和不患有 (n = 14) 子宫内膜异位症的女性样本进行免疫组织化学分析。患有子宫内膜异位症的女性样本包括在位子宫内膜 (n = 20) 样本、浅表子宫内膜异位种植体 (SUP, n = 10)、深层浸润子宫内膜异位种植体 (DIE, n = 15) 和卵巢子宫内膜瘤 (OMA, n = 15)。使用组织分数量化免疫反应性。无论月经周期阶段如何，患有子宫内膜异位症的女性与未患有子宫内膜异位症的女性在位子宫内膜基质中的 KISS1 和 KISS1R 免疫反应性均显着降低（分别为 P = 0.001 和 P = 0.015）。在子宫内膜异位种植体中，与 SUP 相比，DIE (P < 0.01) 和 OMA (P < 0.01) 的腺体和基质成分中 KISS1 水平均显着降低。与 SUP 相比，OMA 腺体成分中的 KISS1R 免疫反应性较低 (P = 0.035)。与未患有子宫内膜异位症的女性相比，在位子宫内膜基质中 KISS1 和 KISS1R 水平较低，这与 KISS1 表达减少在子宫内膜异位症发病机制中的作用一致。由于深层侵袭性病变的 KISS1 水平低于浅表性病变，因此 KISS1 水平的下调可能会导致种植体侵袭性。
Endometriosis is characterized by the presence of ectopic endometrial tissues. Mechanisms of tissue dissemination in endometriosis may be similar to those involved in tumor metastasis. We hypothesize that dysregulation of kisspeptin (KISS1), a metastasis suppressor in endometrial carcinoma, may contribute to the pathogenesis of endometriosis. In this study, we characterized the immunoreactivity of kisspeptin and its receptor, KISS1R, in eutopic and ectopic endometrial tissue of women with and without endometriosis, in proliferative and secretory menstrual cycle phases. Immunohistochemistry was performed using KISS1 and KISS1R antibodies on samples from women with (n = 35) and without (n = 14) endometriosis. Samples from women with endometriosis included eutopic endometrium (n = 20) samples, superficial endometriotic implants (SUP, n = 10) deep infiltrating endometriotic implants (DIE, n = 15), and ovarian endometriomas (OMA, n = 15). Immunoreactivity was quantified using histoscores. KISS1 and KISS1R immunoreactivity was significantly lower in eutopic endometrial stroma of women with versus without endometriosis, regardless of the menstrual cycle phase (P = 0.001 and P = 0.015 respectively). In endometriotic implants, KISS1 levels were significantly lower in both glandular and stromal components of DIE (P < 0.01) and OMA (P < 0.01) compared to SUP. KISS1R immunoreactivity was lower in the glandular component of OMA (P = 0.035) compared to SUP. KISS1 and KISS1R levels are lower in eutopic endometrial stroma from women with versus without endometriosis, consistent with a role for decreased KISS1 expression in the pathogenesis of endometriosis. As deeply invasive lesions showed lower KISS1 levels than superficial lesions, downregulation of KISS1 levels may contribute to implant invasiveness.