Ishimatsu Nana, Miyamoto Tetsu, Ueno Hiromichi, Hasegawa Emi, Kuma Akihiro, Fujimoto Yoko, Bando Kenichiro, Nakamata Junichi, Furuno Yumi, Serino Ryota, Baba Ryoko, Morimoto Hiroyuki, Doi Yoshiaki, Tamura Masahito, Otsuji Yutaka
The Second Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Iseigaoka, Yahatanishi, Kitakyushu, Japan.
Department of Anatomy, School of Medicine, University of Occupational and Environmental Health, Iseigaoka, Yahatanishi, Kitakyushu, Japan.
Histol Histopathol. 2016 Nov;31(11):1251-8. doi: 10.14670/HH-11-756. Epub 2016 Mar 15.
Continuous exposure to peritoneal dialysis fluids (PDFs) is associated with pathological responses such as persistent micro-inflammation, which leads to ultrafiltration failure. Pentraxin-3 (PTX3), a multifunctional soluble pattern recognition receptor, is produced at sites of inflammation by a wide range of cell types. This study investigates the in vivo expression of PTX3 in the peritoneal membrane of a rat continuous peritoneal dialysis (PD) model, as well as the effect of high glucose on the in vitro expression of PTX3.
The expression of PTX3 was analyzed using RT-PCR, real-time PCR, immunohistochemistry and western blotting in a PD rat model receiving saline or conventional PDF containing 3.86% glucose for 8 weeks. The effects of high glucose on the expression of PTX3 were examined in cultured rat peritoneal mesothelial cells (RPMCs), mouse macrophage-like cells, and mouse fibroblasts.
In a rat model of PD, eight-week instillation of the conventional PDF produced increased submesothelial thickening, followed by substantially enhanced PTX3 protein levels in the submesothelial layer of peritoneal membrane. PTX3 was detected in peritoneal mesothelial cells, macrophages and fibroblasts in the thickened submesothelial area. Glucose was found to induce PTX3 protein expression in RPMCs as well as macrophage-like cells and fibroblasts.
Continuous exposure to conventional PDF induces PTX3 expression in the peritoneal membrane of rats. High glucose may be involved in the mechanism of PDF-induced local micro-inflammation in the peritoneum.
持续接触腹膜透析液(PDF)与诸如持续性微炎症等病理反应相关,而持续性微炎症会导致超滤失败。五聚体-3(PTX3)是一种多功能可溶性模式识别受体,由多种细胞类型在炎症部位产生。本研究调查了PTX3在大鼠持续性腹膜透析(PD)模型腹膜中的体内表达情况,以及高糖对PTX3体外表达的影响。
在接受生理盐水或含3.86%葡萄糖的传统PDF治疗8周的PD大鼠模型中,使用逆转录-聚合酶链反应(RT-PCR)、实时定量PCR、免疫组织化学和蛋白质免疫印迹法分析PTX3的表达。在培养的大鼠腹膜间皮细胞(RPMC)、小鼠巨噬细胞样细胞和小鼠成纤维细胞中检测高糖对PTX3表达的影响。
在PD大鼠模型中,传统PDF滴注8周导致皮下增厚增加,随后腹膜膜皮下层的PTX3蛋白水平大幅提高。在增厚的皮下区域的腹膜间皮细胞、巨噬细胞和成纤维细胞中检测到PTX3。发现葡萄糖可诱导RPMC以及巨噬细胞样细胞和成纤维细胞中PTX3蛋白的表达。
持续接触传统PDF可诱导大鼠腹膜中PTX3的表达。高糖可能参与了PDF诱导的腹膜局部微炎症机制。