Ibrahim Mohamed Gamal, Sillem Martin, Plendl Johanna, Chiantera Vito, Sehouli Jalid, Mechsner Sylvia
1 Clinic for Gynaecology, Charité University of Medicine, Hindenburgdamm, Berlin, Germany.
2 Praxisklinik am Rosengarten, Augustaanlage, Mannheim, Germany.
Reprod Sci. 2017 Oct;24(10):1410-1418. doi: 10.1177/1933719116687855. Epub 2017 Jan 17.
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 β1 [TGFβ1] 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.
To study if myofibroblasts-as an evidence of tissue microtrauma-are more abundant at EMJZ in AM-uteri, a case-control experimental study was carried out at Charité University Hospital-Endometriosis 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-β 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.
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.
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.
子宫腺肌病（AM）患者的子宫表现出蠕动亢进。后者会在子宫内膜-肌层交界区（EMJZ）造成慢性组织损伤。组织损伤时，肌层的微小裂隙会促使基底子宫内膜碎片转移至肌层。在那里，会发生化生（由转化生长因子β1 [TGFβ1] 和结缔组织生长因子 [CTGF] 介导）并形成AM病灶。组织中肌成纤维细胞数量丰富是化生的标志，也表明存在组织微创伤。
为研究作为组织微创伤证据的肌成纤维细胞在AM子宫的EMJZ处是否更为丰富，在柏林夏里特大学医院子宫内膜异位症研究中心开展了一项病例对照实验研究。在腹腔镜辅助下经阴道子宫切除术过程中，共获取了18例AM子宫和14例非AM子宫。研究了肌成纤维细胞化生（α平滑肌肌动蛋白 [ASMA] 和I型胶原）、分化型平滑肌标志物（结蛋白）以及化生介质（TGF-β受体1、2、3和CTGF）的免疫标记情况。除了一项体外研究以表征非AM子宫内膜中的肌成纤维细胞外，还通过透射电子显微镜对AM子宫EMJZ处的肌成纤维细胞超微结构进行了表征。
与非AM子宫相比，AM子宫EMJZ处ASMA和I型胶原的免疫标记显著更高。此外，对AM子宫EMJZ处的肌成纤维细胞进行了超微结构表征。非AM子宫的子宫内膜有5%至8%的细胞表达ASMA和I型胶原。两组之间化生介质免疫标记方面未发现差异。
AM子宫EMJZ处丰富且持续存在的肌成纤维细胞（表达ASMA/I型胶原）是慢性组织损伤的超微/微观证据。它们起源于非肌层，因为缺乏结蛋白免疫标记。
