Human Monocyte-Derived Macrophages (MDM): Model 1 (GM-CSF)
Claudia AlteriLorenzo PiermatteoFrancesca Ceccherini‐SilbersteinValentina SvicherCarlo Federico Perno
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Monocyte-to-M0/M1 macrophage differentiation with unclear molecular mechanisms is a pivotal cellular event in many cardiovascular diseases including atherosclerosis. Long non-coding RNAs (lncRNAs) are a group of protein expression regulators; however, the roles of monocyte-lncRNAs in macrophage differentiation and its related vascular diseases are still unclear. The study aims to investigate whether the novel leukocyte-specific lncRNA Morrbid could regulate macrophage differentiation and atherogenesis. We identified that Morrbid was increased in monocytes and arterial walls from atherosclerotic mouse and from patients with atherosclerosis. In cultured monocytes, Morrbid expression was markedly increased during monocyte to M0 macrophage differentiation with an additional increase during M0 macrophage-to-M1 macrophage differentiation. The differentiation stimuli-induced monocyte-macrophage differentiation and the macrophage activity were inhibited by Morrbid knockdown. Moreover, overexpression of Morrbid alone was sufficient to elicit the monocyte-macrophage differentiation. The role of Morrbid in monocyte-macrophage differentiation was also identified in vivo in atherosclerotic mice and was verified in Morrbid knockout mice. We identified that PI3-kinase/Akt was involved in the up-regulation of Morrbid expression, whereas s100a10 was involved in Morrbid-mediated effect on macrophage differentiation. To provide a proof of concept of Morrbid in pathogenesis of monocyte/macrophage-related vascular disease, we applied an acute atherosclerosis model in mice. The results revealed that overexpression of Morrbid enhanced but monocyte/macrophage-specific Morrbid knockout inhibited the monocytes/macrophages recruitment and atherosclerotic lesion formation in mice. The results suggest that Morrbid is a novel biomarker and a modulator of monocyte-macrophage phenotypes, which is involved in atherogenesis.
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Granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) are two important granulopoietic growth factors. This review will focus on the endogenous production of human GM-CSF and human G-CSF and its possible reflection in circulating levels in peripheral blood. When adequately stimulated a variety of cell-types such as monocytes/macrophages. T-lymphocytes, endothelial cells and fibroblasts can produce CSFs in vitro. G-CSF can increase to detectable levels in peripheral blood when there is a demand for granulocyte production such as acute neutropenia in conjunction with hematological disorders, chronic neutropenic conditions and acute infectious diseases in patients with or without underlying hematological disorders. G-CSF in peripheral blood is detected more often and in higher concentrations than GM-CSF. An independent regulation of GM-CSF and G-CSF secretion, quantitative differences in production and/or differences in elimination or distribution might be of importance.
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After infection of mice with Listeria monocytogenes, elevated levels of colony-stimulating factors (CSFs) in the serum were quantitated by six different assays: ability to stimulate colony formation, the proliferation of 2 suspension of bone marrow cells (both measuring total colony-stimulating activity), a radioimmunoassay for macrophage-CSF (CSF-1), the WEHI-3B differentiation assay for granulocyte-CSF, and proliferation of 32D-c1-3 and FDC-P1 cell lines (specific for multi-CSF and either multi- or granulocyte-macrophage-CSFs, respectively). The great bulk of serum colony-stimulating activity represented macrophage- and granulocyte-CSFs, with small but measurable amounts of granulocyte-macrophage-CSF. The degree of elevation of serum CSF depended on the infecting dose used and the numbers of bacteria growing in the spleens and livers of the two mouse strains compared, i.e., L. monocytogenes-resistant C57BL/10 and susceptible BALB/cJ. The increase in serum CSFs occurred before the peak in bone marrow granulocyte-macrophage progenitors and before the reduction in bacterial numbers which follows the onset of specific cell-mediated immunity.
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It is now generally recognized that atherosclerosis is an inflammatory disease,in which monocyte/macrophage plays a crucial role.The monocyte/macrophage is involved in every stage of atherosclerosis.The activity of monocyte/macrophage and their interactions with other cells in the plaque mileu provide novel therapeutic targets for the treatment of atherosclerosis.This paper reviews the recent advances in the treatment of atherosclerosis from those aspects of reducing monocyte/macrophage,suppressing oxidative stress, regulating cholesterol metabolism involved in monocyte/macrophage activities,decreasing macrophage-derived inflammatory activity and increasing plaque stability,to provide a reference for anti-atherosclerosis drugs' clinical use,research and development.
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