Article Text

GW24-e1872 Oxidised low-density lipoprotein induces inflammatory responses in cultured human mast cells via Toll-like receptor 4
  1. Meng Zhe,
  2. Yan Chao,
  3. Dong Xin,
  4. Duan Zongming,
  5. Gao Dengfeng
  1. Department of Cardiology, The Second Affiliated Hospital, Xi’an Jiaotong University School of Medicine


Objectives Oxidized low-density lipoprotein (ox-LDL) is a powerful atherogenic factor during atherosclerosis. Toll-like receptor 4 (TLR4) has a pathophysiological role in regulating the inflammatory responses and atherosclerosis. Mast cells can infiltrate in the atheromatous plaque and secrete various pro-inflammatory cytokines, which significantly amplify the atherogenic processes and promote plaque vulnerability. We evaluated whether ox-LDL-induced inflammation depended in part on the activation of TLR4-dependent signalling pathway in cultured human mast cell line (HMC-1).

Methods HMC-1 cells were cultured, and treated with ox-LDL or inhibitors of TLR4, phosphorylation of the mitogen-activated protein kinase (MAPKs), or nuclear factor-κB (NF-κB). The expressions of monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-α (TNF-α) and interleukin 6 (IL-6) were measured after these treatment.

Results Ox-LDL increased the expression of TLR4 and secretion of MCP-1, TNF-α and IL-6. Moreover, ox-LDL stimulated the transport of NF-κB, a critical mediator of inflammation, from the cytoplasm into nucleus. As well, phosphorylation of the MAPKs pathway was greatly increased. These ox-LDL-induced alterations were significantly attenuated by pretreatment with TLR4-siRNA.

Conclusions Ox-LDL may induce inflammatory responses in cultured HMC-1 cells to cause NF-κB nuclear translocation and phosphorylation of the MAPKs pathway, a process mediated in part by TLR4.

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