Hodge Alexander, Lourensz Dinushka, Vaghjiani Vijesh, Nguyen Huyen, Tchongue Jorge, Wang Bo, Murthi Padma, Sievert William, Manuelpillai Ursula
Centre for Inflammatory Diseases, Monash University, Melbourne, Australia; Gastroenterology and Hepatology Unit, Monash Health, Melbourne, Australia.
Centre for Genetic Diseases, Monash Institute of Medical Research, Monash University, Melbourne, Australia.
Cytotherapy. 2014 Aug;16(8):1132-44. doi: 10.1016/j.jcyt.2014.01.005. Epub 2014 Mar 15.
Intravenous infusion of human amniotic epithelial cells (hAECs) has been shown to ameliorate hepatic fibrosis in murine models. Hepatic stellate cells (HSCs) are the principal collagen-secreting cells in the liver. The aim of this study was to investigate whether factors secreted by hAECs and present in hAEC-conditioned medium (CM) have anti-fibrotic effects on activated human HSCs.
Human AECs were isolated from the placenta and cultured. Human hepatic stellate cells were exposed to hAEC CM to determine potential anti-fibrotic effects.
HSCs treated for 48 h with hAEC CM displayed a significant reduction in the expression of the myofibroblast markers α-smooth muscle actin and platelet-derived growth factor. Expression of the pro-fibrotic cytokine transforming growth factor-β1 (TGF-β1) and intracellular collagen were reduced by 45% and 46%, respectively. Human AEC CM induced HSC apoptosis in 11.8% of treated cells and reduced HSC proliferation. Soluble human leukocyte antigen-G1, a hAEC-derived factor, significantly decreased TGF-β1 and collagen production in activated HSCs, although the effect on collagen production was less than that of hAEC CM. The reduction in collagen and TGF-B1 could not be attributed to PGE2, relaxin, IL-10, TGF-B3, FasL or TRAIL.
Human AEC CM treatment suppresses markers of activation, proliferation and fibrosis in human HSCs as well as inducing apoptosis and reducing proliferation. Human AEC CM treatment may be effective in ameliorating liver fibrosis and warrants further study.
静脉输注人羊膜上皮细胞(hAECs)已被证明可改善小鼠模型中的肝纤维化。肝星状细胞(HSCs)是肝脏中主要的胶原分泌细胞。本研究的目的是调查hAECs分泌并存在于hAEC条件培养基(CM)中的因子是否对活化的人HSCs具有抗纤维化作用。
从胎盘中分离并培养人AECs。将人肝星状细胞暴露于hAEC CM中以确定潜在的抗纤维化作用。
用hAEC CM处理48小时的HSCs显示肌成纤维细胞标志物α-平滑肌肌动蛋白和血小板衍生生长因子的表达显著降低。促纤维化细胞因子转化生长因子-β1(TGF-β1)和细胞内胶原的表达分别降低了45%和46%。人AEC CM诱导11.8%的处理细胞发生HSC凋亡并减少HSC增殖。可溶性人白细胞抗原-G1,一种hAEC衍生因子,显著降低活化HSCs中TGF-β1和胶原的产生,尽管对胶原产生的影响小于hAEC CM。胶原和TGF-B1的减少不能归因于PGE2、松弛素、IL-10、TGF-B3、FasL或TRAIL。
人AEC CM处理可抑制人HSCs中的活化、增殖和纤维化标志物,同时诱导凋亡并减少增殖。人AEC CM处理可能对改善肝纤维化有效,值得进一步研究。