Myofibroblasts Are Evidence of Chronic Tissue Microtrauma at the Endometrial-Myometrial Junctional Zone in Uteri With Adenomyosis
Myofibroblasts Are Evidence of Chronic Tissue Microtrauma at the Endometrial-Myometrial Junctional Zone in Uteri With Adenomyosis
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DOI：
10.1177/1933719116687855
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发表时间：
2017-10-01
影响因子：
2.9
通讯作者：
Mechsner, Sylvia
中科院分区：
文献类型：
--
作者：
Ibrahim, Mohamed Gamal;Sillem, Martin;Mechsner, Sylvia
背景：子宫腺肌病（AM）表现为子宫肥大。后者导致尿道-子宫肌层交界区（EMJZ）的慢性组织创伤。在组织创伤时，子宫肌层的微裂促进了基底子宫内膜碎片移位到子宫肌层。在那里，发生化生（由转化生长因子1 [TGF 1]和结缔组织生长因子[CTGF]介导），并形成AM病变。肌成纤维细胞在组织中的丰富标志着化生，并指出组织microtraumature.Materials和方法：研究如果肌成纤维细胞作为组织microtraumaare更丰富的证据在EMJZ在AM子宫，病例对照实验研究进行了Charite大学医院子宫内膜异位症研究中心。在腹腔镜辅助阴式子宫切除术中，共获得18个AM子宫和14个无AM子宫。研究了肌纤维母细胞化生（α平滑肌肌动蛋白[ASMA]和胶原蛋白I）、分化的平滑肌标志物（结蛋白）和化生介质（TGF-受体1、2、3和CTGF）的免疫标记。在EMJZ的AM子宫肌成纤维细胞的超微结构的特点是通过透射电镜，除了在体外研究，以表征肌成纤维细胞在子宫内膜的非AM uterus.Results：ASMA和胶原蛋白I的免疫标记显着高于EMJZ的AM子宫与非AM uteri。此外，肌成纤维细胞的超微结构特征在EMJZ的AM。非AM子宫的子宫内膜显示其细胞的5%至8%，表达ASMA和胶原I。两组之间的化生介质免疫标记没有差异，注意到：丰富和持久的肌成纤维细胞（表达ASMA/胶原I）在EMJZ在AM子宫是慢性组织创伤的超/显微镜证据。它们是非子宫肌层起源的，因为它们缺乏结蛋白免疫标记。
Background: Adenomyosis (AM) uteri exhibit hyperperistalsis. The latter causes a chronic tissue trauma at the endometrial-myometrial junctional zone (EMJZ). Upon tissue trauma, microdehiscences in the myometrium facilitate the translocation of basal endometrial fragments into the myometrium. There, a metaplasia (mediated by transforming growth factor 1 [TGF1] and connective tissue growth factor [CTGF]) occurs and AM lesions develop. The abundance of myofibroblasts in a tissue hallmarks metaplasia and points to a tissue microtrauma.Materials and Methods: To study if myofibroblastsas an evidence of tissue microtraumaare more abundant at EMJZ in AM-uteri, a case-control experimental study was carried out at Charite University HospitalEndometriosis Research Centre. In all, 18 uteri with AM and 14 uteri without AM were obtained during laparoscopy-assisted vaginal hysterectomy. The immunolabeling of myofibroblastic metaplasia (alpha smooth muscle actin [ASMA] and collagen I), differentiated smooth muscle marker (desmin) and metaplasia mediators (TGF- receptors 1, 2, 3 and CTGF) was investigated. The ultrastructure of myofibroblasts at EMJZ of AM uterus was characterized by transmission electron microscopy, in addition to an in vitro study to characterize myofibroblasts in the endometrium of non-AM uterus.Results: Immunolabeling of ASMA and collagen I was significantly higher at EMJZ of AM uteri versus non-AM uteri. Furthermore, myofibroblasts were ultrastructurally characterized at EMJZ of AM. Endometrium of non-AM uterus exhibited 5% to 8% of its cells, expressing ASMA and collagen I. No difference was noted regarding metaplasia mediators immunolabeling between both the groups.Conclusion: The abundant and persistent myofibroblasts (expressing ASMA/collagen I) at EMJZ in AM uteri are ultra-/microscopic evidence of chronic tissue trauma. They are of nonmyometrial origin, as they lack desmin immunolabeling.