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The effect of lysophosphatidic acid on Toll-like receptor 4 expression and the nuclear factor-κB signaling pathway in THP-1 cells.

Abstract：

:Toll-like receptors (TLRs) are major receptors that mediate the innate immune and inflammatory responses, of which TLR4 has been found most closely related to human atherosclerosis. After ligands are polymerized and activated by TLR, the mitogen-activated protein kinase and nuclear factor-κB (NF-κB) pathways are activated, leading to promotion of NF-κB-regulated transcription of inflammatory factors, thus playing a role in the physiological and pathological processes in atherosclerosis. Oxidized lipoproteins or their components, oxidized lipids, have been confirmed as endogenous TLR receptors. Lysophosphatidic acid (LPA) is an active component of low-density lipoprotein that induces vascular endothelial lesions. However, the mechanism of the TLR4/NF-κB signaling system involved in LPA-induced atherosclerosis has not been fully elucidated. In this study, we investigated the effects of LPA on TLR4 expression, nuclear translocation of NF-κB p65 subunit, and changes in the cytokine tumor necrosis factor α (TNF-α) in human THP-1 cells. LPA upregulated expression of the TLR4 mRNA and protein in THP-1 cells in a dose- and time-dependent manner, induced NF-κB p65 activation synchronously in THP-1 cells, and increased TNF-α secretion. After TLR4 was blocked using TLR4 monoclonal antibody, NF-κB p65 expression and TNF-α secretion were inhibited significantly. These data suggest that LPA can significantly upregulate TLR4 expression and promote NF-κB activation and proinflammatory cytokine secretion in THP-1 cells; it is possible that the TLR4/NF-κB signaling pathway mediates the atherogenic effect of LPA.

journal_name

Mol Cell Biochem

journal_title

Molecular and cellular biochemistry

authors

Yang B,Zhou Z,Li X,Niu J

doi

10.1007/s11010-016-2804-0

subject

Has Abstract

pub_date

2016-11-01 00:00:00

pages

41-49

issue

1-2

eissn

0300-8177

issn

1573-4919

pii

10.1007/s11010-016-2804-0

journal_volume

422

pub_type

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