Nam Bo Young, Park Jung Tak, Kwon Young Eun, Lee Jung Pyo, Jung Jong Ha, Kim Youndong, Kim Seonghun, Park Jimin, Um Jae Eun, Wu Meiyan, Han Seung Hyeok, Yoo Tae-Hyun, Kang Shin-Wook
Severance Biomedical Science Institute, College of Medicine, Yonsei University, Seoul 120-752, Korea.
Department of Internal Medicine, College of Medicine, Brain Korea 21 PLUS, Institute of Kidney Disease Research, Yonsei University, Seoul 120-752, Korea.
Mol Ther Nucleic Acids. 2017 Jun 16;7:396-407. doi: 10.1016/j.omtn.2017.05.001. Epub 2017 May 8.
Peritoneal fibrosis is a major complication in peritoneal dialysis (PD) patients, which leads to dialysis discontinuation. Periostin, increased by transforming growth factor β1 (TGF-β1) stimulation, induces the expression of extracellular matrix (ECM) genes. Aberrant periostin expression has been demonstrated to be associated with PD-related peritoneal fibrosis. Therefore, the effect of periostin inhibition by an aptamer-based inhibitor on peritoneal fibrosis was evaluated. In vitro, TGF-β1 treatment upregulated periostin, fibronectin, α-smooth muscle actin (α-SMA), and Snail expression and reduced E-cadherin expression in human peritoneal mesothelial cells (HPMCs). Periostin small interfering RNA (siRNA) treatment ameliorated the TGF-β1-induced periostin, fibronectin, α-SMA, and Snail expression and restored E-cadherin expression in HPMCs. Similarly, the periostin-binding DNA aptamer (PA) also attenuated fibronectin, α-SMA, and Snail upregulation and E-cadherin downregulation in TGF-β1-stimulated HPMCs. In mice treated with PD solution for 4 weeks, the expression of periostin, fibronectin, α-SMA, and Snail was significantly increased in the peritoneum, whereas E-cadherin expression was significantly decreased. The thickness of the submesothelial layer and the intensity of Masson's trichrome staining in the PD group were significantly increased compared to the untreated group. These changes were significantly abrogated by the intraperitoneal administration of PA. These findings suggest that PA can be a potential therapeutic strategy for peritoneal fibrosis in PD patients.
腹膜纤维化是腹膜透析(PD)患者的主要并发症,可导致透析中断。骨膜蛋白在转化生长因子β1(TGF-β1)刺激下增加,可诱导细胞外基质(ECM)基因的表达。已证明骨膜蛋白异常表达与PD相关的腹膜纤维化有关。因此,评估了基于适体的抑制剂抑制骨膜蛋白对腹膜纤维化的影响。在体外,TGF-β1处理上调了人腹膜间皮细胞(HPMC)中骨膜蛋白、纤连蛋白、α-平滑肌肌动蛋白(α-SMA)和Snail的表达,并降低了E-钙黏蛋白的表达。骨膜蛋白小干扰RNA(siRNA)处理改善了TGF-β1诱导的HPMC中骨膜蛋白、纤连蛋白、α-SMA和Snail的表达,并恢复了E-钙黏蛋白的表达。同样,骨膜蛋白结合DNA适体(PA)也减弱了TGF-β1刺激的HPMC中纤连蛋白、α-SMA和Snail的上调以及E-钙黏蛋白的下调。在用PD溶液处理4周的小鼠中,腹膜中骨膜蛋白、纤连蛋白、α-SMA和Snail的表达显著增加,而E-钙黏蛋白的表达显著降低。与未处理组相比,PD组的间皮下层厚度和Masson三色染色强度显著增加。腹腔内注射PA可显著消除这些变化。这些发现表明,PA可能是PD患者腹膜纤维化的一种潜在治疗策略。