期刊论文详细信息
Biological research: BR
Human amnion mesenchymal cells inhibit lipopolysaccharide-induced TNF-α and IL-1β production in THP-1 cells
Xiaojuan He1  Jun Shu2  Xiaojie Huang2  Lan Zhang2  Hong Li2  Ping Wang2 
[1] Institute of Basic Research in Clinical Medicine, China Academy of Chinese Medical Sciences, Beijing, China;Institute of Clinical Medical Science, China-Japan Friendship Hospital, Beijing, China
关键词: Human amnion mesenchymal cells;    THP-1 cells;    TNF-α;    IL-1β;    Immunosuppression;   
DOI  :  10.1186/s40659-015-0062-3
学科分类:生物科学(综合)
来源: BioMed Central
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【 摘 要 】

Human amnion mesenchymal cells (hAMCs), isolated from the amniotic membrane of human placenta, are a unique population of mesenchymal stem cells. Recent studies demonstrated that hAMCs could inhibit the activities and functions of several immune cells. However, their effect on inflammatory macrophages is largely unknown. This study investigated the effect of hAMCs on expression of inflammatory cytokines and mitogen-activated protein kinases (MAPKs)/NF-κB pathway in human THP-1 macrophages induced by lipopolysaccharide (LPS). The levels of TNF-α and IL-1β secreted by LPS- stimulated THP-1 cells were increased significantly compared with those in the control group. After co-culture with different numbers of hAMCs, the levels of TNF-α and IL-1β in LPS-stimulated THP-1 cells were significantly reduced compared with the LPS group. The mRNA expression of TNF-α and IL-1β were also markedly inhibited. Moreover, treating LPS-stimulated THP-1 cells with hAMCs supernatants could also suppress TNF-α and IL-1β production in THP-1 cells. Important signaling pathways involved in the production of TNF-α and IL-1β were affected by hAMCs co-culture: hAMCs remarkably suppressed NF-κB activation and down-regulated the phosphorylation of ERK and JNK in LPS- stimulated THP-1 cells. Human amnion mesenchymal cells inhibited the production of TNF-α and IL-1β secreted by LPS-stimulated THP-1 cells, partly through the suppression of NF-κB activation and ERK and JNK phosphorylation.

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