趋化因子
系膜细胞
巨噬细胞极化
细胞生物学
血小板源性生长因子受体
巨噬细胞
化学
系膜
巨噬细胞集落刺激因子
细胞因子
炎症
血小板衍生生长因子
M2巨噬细胞
生长因子
癌症研究
肾小球肾炎
内分泌学
免疫学
生物
肾
体外
受体
生物化学
作者
Wu-Qiong Liao,Shaoyuan Cui,Qing Ouyang,Yan Mei,Guangyan Cai,Bo Fu,Qian Ma,Xueyuan Bai,Qinggang Li,Xiangmei Chen
出处
期刊:Journal of Interferon and Cytokine Research
[Mary Ann Liebert]
日期:2018-12-01
卷期号:38 (12): 566-577
被引量:6
标识
DOI:10.1089/jir.2018.0093
摘要
Mesangial cell (MC) activation and macrophage infiltration are 2 major events closely related with each other in mesangial proliferative glomerulonephritis. In the anti-Thy 1 nephritis model, macrophages mediate the damage and also the expansion of mesangium through secreting various inflammatory factors; however, in glomerular microenvironment how MCs affect macrophage activity in the presence of various stimuli have not yet been understood. In the present study, we found that resting human MCs (HMCs) constitutively expressed chemokine [C-C motif] ligand 2 (CCL-2) and interleukin (IL)-6 and induced M2 polarization of macrophages in the coculture system. HMC proliferation and migration and expression of IL-6, CCL-2, and macrophage colony-stimulating factor in HMCs were enhanced after platelet-derived growth factor (PDGF)-BB stimulation, among which CCL-2 was responsible for inducing the M2 polarization of macrophages. Furthermore, PDGF-BB-stimulated HMCs alleviated the classical activation of macrophages and drove more intensified M2 polarization of macrophages than resting HMCs did. However, lipopolysaccharide and interferon-γ (IFN-γ) stimulated HMCs maintained the M1 phenotype of cocultured macrophages. In conclusion, MCs actively participated in glomerular inflammation through influencing macrophage polarization. The interplay between MCs and infiltrated macrophages is finely modulated by secretory factors such as PDGF-BB and IFN-γ in response to the renal inflammatory microenvironment.
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