tenascin-C在早期腹膜子宫内膜异位症病灶形成中的作用。

Maako Moriyama M.D. , Kazuomi Nakamura Ph.D. , Hiroki Nagata M.D. , Ikumi Wada M.D. , Kei Nagira M.D., Ph.D. , Yukihiro Azuma M.D., Ph.D. , Eri Sato M.D., Ph.D. , Tasuku Harada M.D., Ph.D. , Fuminori Taniguchi M.D., Ph.D.
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引用次数: 0

摘要

目的确定有助于子宫内膜异位症早期病变近端粘附和侵入腹膜的细胞因子或细胞外基质(ECM)成分:设计:实验室研究患者和动物:五名患有卵巢子宫内膜异位症的妇女:5名患有卵巢子宫内膜异位症的妇女、138只野生型(WT)C57BL/6N小鼠和48只Tenascin C(Tnc)基因敲除(TncKO)小鼠:干预措施:为了建立小鼠子宫内膜异位症模型,给合成小鼠腹腔注射每个子宫角的20块碎子宫组织片段。三天后,收集子宫内膜异位症病灶和腹膜组织。另外,我们用Tnc小干扰RNA(siRNA)转染人腹膜间皮细胞(HMrSV5)或人子宫内膜基质细胞(hESCs):我们采用PCR阵列分析了小鼠腹膜中的基因表达,包括病变远端腹膜(PDL)和子宫内膜异位症病变周围腹膜(PSL)。通过实时 RT-PCR 在腹膜样本中验证了 PSL 中上调基因的表达。我们利用 TncKO 小鼠来研究 Tnc 在子宫内膜异位症发病过程中的作用。我们通过 Ki-67 或 CD3 免疫染色法评估了病灶的增殖活性或炎症状态。通过荧光激活细胞分拣(FACS)评估了巨噬细胞在腹腔内的分布。我们使用 Tnc siRNA 检测了 hESCs 与 HMrSV5 共培养系统中的侵袭能力:结果:Tnc基因在PSL中的表达明显高于PDL。TncKO宿主中TncKO病灶的重量和数量低于WT宿主中WT病灶的重量和数量。相反,TncKO宿主体内未附着的TncKO病变的重量和数量高于WT宿主体内未附着的WT病变。我们观察到,在TncKO受体的TncKO病灶中,Ki-67阳性细胞或CD3的H-scores减少,M1巨噬细胞比例降低,M2巨噬细胞比例升高。抑制Tnc在hESCs和HMrSV5中的表达可降低hESCs的侵袭性:结论:Tnc可能是早期腹膜子宫内膜异位症发生的关键因素。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Role of tenascin C in lesion formation in early peritoneal endometriosis

Objective

To identify cytokines or extracellular matrix components that contribute to adhesion to, and invasion of, the peritoneum, proximal to lesions in the early phase of endometriosis.

Design

Laboratory-based study.

Setting

University Hospital and Laboratory of Animal Science.

Patients and Animals

Five women with ovarian endometrioma, 138 wild-type (WT) C57BL/6N mice, and 48 Tenascin C (Tnc) knockout (TncKO) mice.

Interventions

To establish a murine endometriosis model, 20 pieces of minced uterine tissue fragments from each horn were administered intraperitoneally to syngeneic mice. Three days later, endometriotic lesions and peritoneal tissues were collected. Separately, we transfected human peritoneal mesothelial cells (HMrSV5) or human endometrial stromal cells (hESCs) with Tnc small interfering ribonucleic acid.

Main Outcome Measures

We employed a polymerase chain reaction array to profile gene expression in the murine peritoneum, in both peritoneum distal to lesions and peritoneum surrounding lesions (PSL). The expression of upregulated genes in the PSL was verified in the peritoneal samples by real-time reverse transcription-polymerase chain reaction. TncKO mice were used to investigate the role of Tnc in the development of endometriosis. We evaluated the proliferative activity or inflammatory state of lesions by Ki67 or CD3 immunostaining. Intraperitoneal distribution of macrophages was assessed by fluorescence-activated cell sorting. Using Tnc small interfering ribonucleic acid, we examined the invasive capacity of hESCs in a coculture system with HMrSV5.

Results

Tnc gene expression was significantly higher in PSL than in peritoneum distal to lesions. The weight and number of TncKO lesions in TncKO hosts were lower than those of WT lesions in WT hosts. In contrast, the weight and number of nonattached TncKO lesions in TncKO hosts were higher than those of nonattached WT lesions in WT hosts. We observed decreased Ki67-positive cells or H-scores for CD3, a lower proportion of M1 macrophages, and a higher proportion of M2 macrophages in TncKO lesions in TncKO recipients. Silencing of Tnc expression in hESCs and HMrSV5 diminished the invasivity of hESCs.

Conclusion

Tnc may be a crucial factor in the development of early peritoneal endometriosis.

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来源期刊
F&S science
F&S science Endocrinology, Diabetes and Metabolism, Obstetrics, Gynecology and Women's Health, Urology
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51 days
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