Cytokine regulation of granulocyte-macrophage colony stimulating factor and macrophage colony-stimulating factor production in human arterial smooth muscle cells

Filonzi, Enríco L.; Zoellner, Hans; Stanton, Heather; Hamilton, John A.

doi:10.1016/0021-9150(93)90026-q

Cited by 79 publications

(48 citation statements)

References 37 publications

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“…In mouse and human lesions, M-CSF is detected both in healthy arteries and atherosclerotic lesions, and in the latter is associated with macrophage and foam-cell content and correlates with plaque progression [8,21,22,34]. These data are consistent with a scenario in which M-CSF and GM-CSF both contribute to macrophage heterogeneity observed in plaques.…”

Section: Stimulation Of Human Cd14supporting

confidence: 79%

Microenviromental factors controlling macrophage polarization in atherosclerosis

Pello¹

2011

Endocrinol Metab Syndr

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Macrophages are critical for the initiation and perpetuation of intravascular inflammation through their ability to produce an array of cytokines and chemokines, to generate reactive oxygen species, and to process and present antigens to CD4 + T cells. Macrophages constitute a heterogeneous population of cells that are distinctly activated by various microenvironmental signals; however, the mechanisms contributing to the generation of distinct macrophage phenotypes in the context of atherosclerosis remain unclear. This review summarizes the well-characterized factors that govern macrophage polarization toward a specific phenotype and function. Understanding the microenviromental factors that control macrophage polarization and the precise roles of distinct macrophage subsets could provide the basis for novel treatment strategies aimed at limiting the progression of atherosclerosis.

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Section: Stimulation Of Human Cd14supporting

confidence: 79%

Microenviromental factors controlling macrophage polarization in atherosclerosis

Pello¹

2011

Endocrinol Metab Syndr

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“…2 The importance of CSF-1 as a maintenance factor for monocytes/macrophages has led to the speculation that it may be required to maintain long-term survival of macrophages in lesions. 8,11,38,39 Even though care must be exercised in extrapolating from these in vitro studies, we suggest that low doses of ox-LDL, and perhaps other modified forms, could maintain macrophage (and foam cell) survival and therefore lengthen their tenure in a lesion by suppressing the apoptotic process with possible consequences for plaque progression. Others have found that ox-LDL (Ն100 g/mL) causes apoptotic death in monocytes/macrophages in vitro, 21,22 and macrophage (foam cell) death has been proposed to contribute to the lipid core of the atheroma.…”

Section: Discussionmentioning

confidence: 97%

Oxidized LDL Can Induce Macrophage Survival, DNA Synthesis, and Enhanced Proliferative Response to CSF-1 and GM-CSF

Hamilton

Myers

Jessup

et al. 1999

ATVB

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126

117

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Abstract-Modification of low density lipoprotein (LDL), eg, by oxidation, has been proposed as being important for the formation of foam cells and therefore for the development of atherosclerotic plaques. There are a number of reports showing that macrophage-derived foam cells can proliferate in both human and animal lesions, particularly in the early phase of the disease and possibly involving macrophage-colony stimulating factor (M-CSF, or CSF-1). We studied the in vitro effects of oxidized LDL (ox-LDL) on murine bone marrow-derived macrophages (BMMs), a cell population with a high proliferative capacity in vitro in response to CSF-1 and a dependence for survival on the presence of this growth factor. We report here that treatment of BMMs with low doses of ox-LDL, but not with native LDL, led to cell survival, DNA synthesis, and an enhanced response to the proliferative actions of CSF-1 and granulocyte macrophage-CSF (GM-CSF); the effects were dependent on the degree of LDL oxidation. For CSF-1, a synergistic effect was noticeable at suboptimal doses. The effect of ox-LDL occurred even in the absence of endogenous CSF-1 or GM-CSF. Our findings suggest that ox-LDL, and possibly other modified forms of LDL, could maintain macrophage (and foam cell) survival and therefore lengthen their tenure in a plaque; the modified LDL could also cause local macrophage proliferation or "prime" them so that they could proliferate better in response to CSF-1 (and GM-CSF) concentrations that may be present in the atheroma.

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“…Although the precise molecular mechanisms of the actions of M-CSF are still unclear, different actions as compared with GM-CSF are envisioned, given different expression patterns in the vascular wall. Whereas M-CSF is constitutively expressed under physiological conditions in endothelial cells, fibroblasts, macrophages and smooth muscle cells, GM-CSF, by contrast, is expressed only in minute amounts in these cells under basal conditions, but instead is induced by inflammatory stimuli (for example, tumour necrosis factor) 45 or oxidized low-density lipoprotein cholesterol stimulation 46 . In murine and human lesions, M-CSF is detected both in healthy arteries and in atherosclerotic lesions associated with macrophage and foam cell content, and is correlated with plaque progression in the latter.…”

Section: Discussionmentioning

confidence: 99%

Granulocyte macrophage colony-stimulating factor is required for aortic dissection/intramural haematoma

et al. 2015

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Aortic dissection and intramural haematoma comprise an aortopathy involving separation of the aortic wall. Underlying mechanisms of the condition remain unclear. Here we show that granulocyte macrophage colony-stimulating factor (GM-CSF) is a triggering molecule for this condition. Transcription factor Krüppel-like factor 6 (KLF6)-myeloid-specific conditional deficient mice exhibit this aortic phenotype when subjected to aortic inflammation. Mechanistically, KLF6 downregulates expression and secretion of GM-CSF. Administration of neutralizing antibody against GM-CSF prevents the condition in these mice. Conversely, administration of GM-CSF in combination with aortic inflammation to wild-type mice is sufficient to induce the phenotype, suggesting the general nature of effects. Moreover, patients with this condition show highly increased circulating levels of GM-CSF, which is also locally expressed in the dissected aorta. GM-CSF is therefore a key regulatory molecule causative of this aortopathy, and modulation of this cytokine might be an exploitable treatment strategy for the condition.

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Cytokine regulation of granulocyte-macrophage colony stimulating factor and macrophage colony-stimulating factor production in human arterial smooth muscle cells

Cited by 79 publications

References 37 publications

Microenviromental factors controlling macrophage polarization in atherosclerosis

Microenviromental factors controlling macrophage polarization in atherosclerosis

Oxidized LDL Can Induce Macrophage Survival, DNA Synthesis, and Enhanced Proliferative Response to CSF-1 and GM-CSF

Granulocyte macrophage colony-stimulating factor is required for aortic dissection/intramural haematoma

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