Macrophage Inflammatory Protein-1β: A Novel Prognostic Biomarker in Atherosclerosis?

Vistnes, Maria

doi:10.1159/000336484

Cited by 8 publications

(8 citation statements)

References 40 publications

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“…Population studies have demonstrated that increased CCL-4 levels are associated with a poor prognosis for coronary heart disease (47–49). Mechanistic analysis has indicated that CCL-4 is increased in atherosclerotic plaques, and reducing its expression or inhibiting it with a CCR-5 antagonist can attenuate the development of atherosclerosis (50). Classically, CCL-4 is regarded as a pro-inflammatory cytokine and mediates the inflammatory cascade, promoting atherosclerotic lesion formation.…”

Section: Discussionmentioning

confidence: 99%

Macrophage-derived foam cells impair endothelial barrier function by inducing endothelial-mesenchymal transition via CCL-4

Yang

Luo

Ren

et al. 2017

International Journal of Molecular Medicine

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Recently, endothelial-mesenchymal transition (EndMT) has been demonstrated to play an important role in the development of atherosclerosis, the molecular mechanisms of which remain unclear. In the present study, scanning electron microscopy directly revealed a widened endothelial space and immunohistofluorescence demonstrated that EndMT was increased in human aorta atherosclerotic plaques. M1 macrophage-derived foam cell (M1-FC) supernatants, but not M2 macrophage-derived foam cell (M2-FC) supernatants, induced EndMT. A protein array and enzyme-linked immunosorbent assay identified that the levels of several cytokines, including C-C motif chemokine ligand 4 (CCL-4) were increased in M1-FC supernatants, in which EndMT was promoted, accompanied by increased endothelial permeability and monocyte adhesion. Furthermore, anti-CCL-4 antibody abolished the effects of M1-FC supernatants on EndMT. At the same time, CCL-4 activated its receptor, C-C motif chemokine receptor-5 (CCR-5), and upregulated transforming growth factor-β (TGF-β) expression. Further experiments revealed that EndMT induced by CCL-4 was reversed by treatment with CCR-5 antagonist and the RNA-mediated knockdown of TGF-β. On the whole, the data of the present study suggest that M1-FCs induce EndMT by upregulating CCL-4, and increase endothelial permeability and monocyte adhesion. These data may help to elucidate the important role of EndMT in the development of atherosclerosis.

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Section: Discussionmentioning

confidence: 99%

Macrophage-derived foam cells impair endothelial barrier function by inducing endothelial-mesenchymal transition via CCL-4

Yang

Luo

Ren

et al. 2017

International Journal of Molecular Medicine

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“…IL-8 and other chemokines have been considered to play a role in developing peripheral artery disease [ 30 ]. Macrophage inflammatory markers (MIP-1α, β) have been determined to be critical factors affecting atherosclerosis [ 31 , 32 ]. A previous study suggested that MIP-1α and β were expressed by infiltrating leukocytes, the renal tubular cells, and peritubular capillaries in patients with kidney diseases [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

Effects of the mTOR inhibitor Rapamycin on Monocyte-Secreted Chemokines

et al. 2014

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BackgroundMammalian target of rapamycin (mTOR) inhibitors, such as sirolimus and its derivative, everolimus, are potent immunosuppressive and antiproliferative drugs. Inflammatory diseases are characterized by immunological dysfunction, and monocyte recruitment underlies the mechanism of cell damage. Chemokines attract inflammatory cells to sites of inflammation. Interleukin-8 (IL-8/CXCL8); the monocyte chemoattractant protein-1 (MCP-1/CCL2); the regulated on activation, normal T cell expressed, presumably secreted protein (RANTES/CCL5); the macrophage inflammatory protein (MIP)-1α (CCL3); and MIP-1β (CCL4) are involved in the pathogenesis of inflammation. However, whether mTOR inhibitors moderate the production of chemokines in monocytes remains unclear.MethodsA human monocyte cell line, THP-1, and primary monocytes obtained from human volunteers, were stimulated using lipopolysaccharide (LPS), and then treated with sirolimus. The expression of the MCP-1, RANTES, IL-8, MIP-1α, MIP-1β, and TNF-α proteins was measured using enzyme-linked immunosorbent assays, and intracellular signalling was examined using western blotting.ResultsSirolimus significantly suppressed the LPS-induced expression of MCP-1, IL-8, RANTES, MIP-1α, and MIP-1β in the THP-1 cells and human primary monocytes. The mitogen-activated protein kinase (MAPK) inhibitors that were examined suppressed the LPS-induced expression of MCP-1, IL-8, RANTES, MIP-1α, and MIP-1β. In addition, sirolimus suppressed the LPS-induced phosphorylation of p38 and p65 in the THP-1 and human primary monocytes.ConclusionSirolimus downregulates the expression of chemokines in monocytes, including MCP-1, RANTES, IL-8, MIP-1α, and MIP-1β, by inhibiting the NF-κB-p65 and MAPK-p38 signalling pathways.

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“…Inflammatory mediators such as interleukins, C-reactive protein [10], mean platelet volume, red blood cell distribution width [11], homocysteine [12] and vascular endothelial growth factor [13] play a pivotal role in atherosclerosis and atherosclerotic complications [14]. As a stand-alone marker, i.e.…”

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confidence: 99%

Cell-Free Circulating DNA as a Novel Biomarker in Patients with the Acute Coronary Syndrome

et al. 2013

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Macrophage Inflammatory Protein-1β: A Novel Prognostic Biomarker in Atherosclerosis?

Cited by 8 publications

References 40 publications

Macrophage-derived foam cells impair endothelial barrier function by inducing endothelial-mesenchymal transition via CCL-4

Macrophage-derived foam cells impair endothelial barrier function by inducing endothelial-mesenchymal transition via CCL-4

Effects of the mTOR inhibitor Rapamycin on Monocyte-Secreted Chemokines

Cell-Free Circulating DNA as a Novel Biomarker in Patients with the Acute Coronary Syndrome

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