The peritoneum is both a source and target of TGF-β in women with endometriosis.
The peritoneum is both a source and target of TGF-β in women with endometriosis.
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DOI：
10.1371/journal.pone.0106773
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Horne AW
中科院分区：
文献类型：
--
作者：
Young VJ;Brown JK;Saunders PT;Duncan WC;Horne AW
转化生长因子-β（TGF-β）被认为在腹膜子宫内膜异位症的病因学中起主要作用。我们的目的是确定腹膜是否是TGF-β的来源，以及腹膜TGF-β的表达、受体或靶基因在子宫内膜异位症患者中是否发生改变。收集子宫内膜异位症患者和非子宫内膜异位症患者的腹膜液、腹膜套管和腹膜活检标本。测定腹腔液中TGF-β1、2和3蛋白浓度。在间皮细胞条件培养基中测量TGF-β1。对照腹膜和来自无疾病女性（n = 16）的易患子宫内膜异位症的腹膜（在道格拉斯囊内）以及患有子宫内膜异位症女性（n = 15）的子宫内膜异位症病灶远端和邻近的腹膜，并通过免疫组织化学、qRT-PCR和TGF-β信号传导PCR阵列分析TGF-β表达、接收和信号传导。 子宫内膜异位症患者腹腔液中TGF-β1的表达明显高于正常对照组（P<0.05），腹膜间皮细胞在体外培养中可分泌TGF-β1。在子宫内膜异位症患者中，邻近病变部位的腹膜组织TGF β 1 mRNA表达水平高于远端部位（P<0.05）。子宫内膜异位症患者腹膜中TGF-β刺激的Smad 2/3信号通路活跃，肿瘤发生相关基因（MAPK 8、CDC 6）、上皮-间质转化相关基因（NOTCH 1）、血管生成相关基因（ID 1、ID 3）和神经发生相关基因（CREB 1）的表达显著增加（P<0.05）。总之，腹膜，特别是腹膜间皮，是TGF-β1的来源，并且在子宫内膜异位症病变周围增强。子宫内膜异位症患者腹膜中TGF-β调节基因的表达发生改变，这可能促进了有利于病变形成的环境。
Transforming growth factor-β (TGF-β) is believed to play a major role in the aetiology of peritoneal endometriosis. We aimed to determine if the peritoneum is a source of TGF-β and if peritoneal TGF-β expression, reception or target genes are altered in women with endometriosis. Peritoneal fluid, peritoneal bushings and peritoneal biopsies were collected from women with and without endometriosis. TGF-β1, 2 and 3 protein concentrations were measured in the peritoneal fluid. TGF-β1 was measured in mesothelial cell conditioned media. Control peritoneum and peritoneum prone to endometriosis (within Pouch of Douglas) from women without disease (n = 16) and peritoneum distal and adjacent to endometriosis lesions in women with endometriosis (n = 15) and were analysed for TGF-β expression, reception and signalling by immunohistochemistry, qRT-PCR and a TGF-β signalling PCR array. TGF-β1 was increased in the peritoneal fluid of women with endometriosis compared to those without disease (P<0.05) and peritoneal mesothelial cells secrete TGF-β1 in-vitro. In women with endometriosis, peritoneum from sites adjacent to endometriosis lesions expressed higher levels of TGFB1 mRNA when compared to distal sites (P<0.05). The TGF-β-stimulated Smad 2/3 signalling pathway was active in the peritoneum and there were significant increases (P<0.05) in expression of genes associated with tumorigenesis (MAPK8, CDC6), epithelial-mesenchymal transition (NOTCH1), angiogenesis (ID1, ID3) and neurogenesis (CREB1) in the peritoneum of women with endometriosis. In conclusion, the peritoneum, and in particular, the peritoneal mesothelium, is a source of TGF-β1 and this is enhanced around endometriosis lesions. The expression of TGF-β-regulated genes is altered in the peritoneum of women with endometriosis and this may promote an environment favorable to lesion formation.
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