Kajiyama Hiroaki, Shibata Kiyosumi, Ino Kazuhiko, Nawa Akihiro, Mizutani Shigehiko, Kikkawa Fumitaka
Department of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Tsurumai-cho 65, Showa-ku, Nagoya, 466-8550, Japan.
Cell Tissue Res. 2007 Nov;330(2):221-9. doi: 10.1007/s00441-007-0455-x. Epub 2007 Sep 11.
We have previously reported that human peritoneal mesothelial cells (HPMCs) express a large amount of dipeptidyl peptidase IV (DPPIV) and that its expression is regulated by a variety of bioactive substances in malignant ascites from ovarian cancer patients. The aim of this study has been to examine the expression and role of the SDF-1alpha/CXCR4-DPPIV axis in HPMCs. We have demonstrated that the expression levels of DPPIV and E-cadherin in HPMCs decrease, following TGF-beta1-induced morphological change, in a time- and concentration-dependent manner. Additionally, we show that both SDF-1alpha (a chemokine and substrate for DPPIV) and its receptor, CXCR4, are expressed on HPMCs, and that their expression levels are upregulated by TGF-beta1 treatment, resulting in an increased migratory potential of HPMCs. Furthermore, the migratory potential of HPMCs is significantly enhanced in the presence of SDF-1alpha or DPPIV-specific inhibitor in the wound-healing assay. These results suggest that DPPIV and SDF-1alpha/CXCR4 play crucial roles in regulating the migratory potential of HPMCs, which may be involved in the re-epithelialization of denuded basement membrane at the site of peritoneal injury.
我们之前报道过,人腹膜间皮细胞(HPMCs)表达大量二肽基肽酶IV(DPPIV),且其表达受卵巢癌患者恶性腹水中多种生物活性物质的调节。本研究的目的是检测SDF-1α/CXCR4-DPPIV轴在HPMCs中的表达及作用。我们已经证明,在转化生长因子-β1(TGF-β1)诱导的形态变化后,HPMCs中DPPIV和E-钙黏蛋白的表达水平呈时间和浓度依赖性下降。此外,我们发现趋化因子SDF-1α(DPPIV的一种底物)及其受体CXCR4均在HPMCs上表达,并且它们的表达水平在TGF-β1处理后上调,从而导致HPMCs的迁移潜能增加。此外,在伤口愈合试验中,SDF-1α或DPPIV特异性抑制剂存在时,HPMCs的迁移潜能显著增强。这些结果表明,DPPIV和SDF-1α/CXCR4在调节HPMCs的迁移潜能中起关键作用,这可能参与腹膜损伤部位裸露基底膜的重新上皮化过程。