Li Juan, Yin Geping, Chen Ming, Yang Shujun, Wu Aifang, Liang Jing, Yuan Zheng
Department of Obstetrics and Gynecology, Jinan Military General Hospital, Jinan, Shandong 250031, P.R. China.
Oncol Lett. 2017 Apr;13(4):2731-2736. doi: 10.3892/ol.2017.5762. Epub 2017 Feb 22.
The aim of the present study was to investigate the role of chemokine (C-X-C motif) ligand 12 (CXCL12) and its receptor, chemokine (C-X-C motif) receptor 4 (CXCR4) in the pathogenesis of adenomyosis (AD). Immunohistochemistry and reverse transcription-quantitative polymerase chain reaction analysis were used to measure the protein and mRNA expression of CXCL12 and CXCR4 in eutopic endometrial and ectopic foci tissue samples. Samples from a total of 36 patients with AD (study group) were compared with endometrial tissue samples from 33 patients who underwent uterine fibroids surgery (control group) during the same period. All data are presented as the mean ± standard deviation and were analyzed with SPSS software (version 16.0). Analysis of variance was used for between group analysis and pairwise comparison was performed using Fisher's least significant difference post hoc test. The results of the present study revealed that CXCL12 and CXCR4 protein expression was significantly increased in ectopic foci tissue compared with eutopic endometrial tissue samples from patients with AD. CXCL12 and CXCR4 protein expression in ectopic foci and eutopic endometrial tissue samples were significantly increased compared with the control group (P<0.05 for between group comparisons). No significant differences were identified in CXCL12 and CXCR4 protein expression between the proliferative and secretory phases within each group. Furthermore, CXCL12 and CXCR4 mRNA expression was significantly increased in ectopic foci tissue and eutopic endometrial tissue compared with the control group (P<0.05 for between group comparisons). CXCL12 mRNA expression was markedly increased in ectopic foci tissue compared with eutopic endometrial tissue of patients with AD. The expression of CXCR4 mRNA was significantly increased in eutopic endometrial tissue compared with ectopic foci tissue and the control group (P<0.05 for between group comparisons). No significant differences were identified in CXCL12 and CXCR4 mRNA expression between proliferative and secretory phase within each group. In conclusion, CXCL12 and CXCR4 may induce the ectopia, and promote the spread and localized growth of endometrial cells in the development of AD.
本研究旨在探讨趋化因子(C-X-C基序)配体12(CXCL12)及其受体趋化因子(C-X-C基序)受体4(CXCR4)在子宫腺肌病(AD)发病机制中的作用。采用免疫组织化学和逆转录-定量聚合酶链反应分析来检测CXCL12和CXCR4在在位内膜和异位病灶组织样本中的蛋白质和mRNA表达。将总共36例AD患者的样本(研究组)与同期33例行子宫肌瘤手术患者的子宫内膜组织样本(对照组)进行比较。所有数据均以均值±标准差表示,并使用SPSS软件(版本16.0)进行分析。方差分析用于组间分析,两两比较采用Fisher最小显著差事后检验。本研究结果显示,与AD患者的在位内膜组织样本相比,异位病灶组织中CXCL12和CXCR4蛋白表达显著增加。与对照组相比,异位病灶和在位内膜组织样本中CXCL12和CXCR4蛋白表达显著增加(组间比较P<0.05)。每组增殖期和分泌期之间CXCL12和CXCR4蛋白表达未发现显著差异。此外,与对照组相比,异位病灶组织和在位内膜组织中CXCL12和CXCR4 mRNA表达显著增加(组间比较P<0.05)。与AD患者的在位内膜组织相比,异位病灶组织中CXCL12 mRNA表达明显增加。与异位病灶组织和对照组相比,在位内膜组织中CXCR4 mRNA表达显著增加(组间比较P<0.05)。每组增殖期和分泌期之间CXCL12和CXCR4 mRNA表达未发现显著差异。总之,CXCL12和CXCR4可能诱导异位,并在AD发生发展过程中促进子宫内膜细胞的扩散和局部生长。