M-CSF stimulated differentiation requires persistent MEK activity and MAPK phosphorylation independent of Grb2–Sos association and phosphatidylinositol 3-kinase activity

Gosse, Stéphanie Gobert; Bourgin, Caroline; Liu, Wang Qing; Garbay, Christiane; Mouchiroud, Guy

doi:10.1016/j.cellsig.2005.02.002

Cited by 45 publications

(59 citation statements)

References 42 publications

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“…For instance, the further upregulation of CD14 and CD163 in macrophages cotreated with M-CSF and IL-32g (Fig. 6) might be explained by the sustained activation of MAPKs, because it has been shown that M-CSF-stimulated differentiation of murine myeloid cell line FD/Fms cells into macrophage-like cells requires persistent activation of MAPKs (41). However, the reason for the delayed signaling activation induced by IL-32g is still unclear, because no IL-32-specific receptor has yet been identified, although IL-32 was reported to interact with integrins such as aVb3 and aVb6 through its Arg-Gly-Asp (RGD) motif (42).…”

Section: Discussionmentioning

confidence: 99%

M-CSF Inhibits Anti–HIV-1 Activity of IL-32, but They Enhance M2-like Phenotypes of Macrophages

Osman

Bhuyan

Hashimoto

et al. 2014

The Journal of Immunology

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M-CSF promotes the differentiation and survival of macrophages, and preferentially induces anti-inflammatory M2, rather than proinflammatory M1 macrophages. Recently, another cytokine, IL-32, was also shown to promote macrophage differentiation. In this article, we provide the first evidence, to our knowledge, that M-CSF has both additive and inhibitory effects on the macrophage-related activities of IL-32. When added to M-CSF–derived macrophages, M-CSF and IL-32 promoted macrophage survival, which was further enhanced by their combination. However, they had different effects on HIV-1 replication; that is, it was stimulated by M-CSF and inhibited by IL-32. Interestingly, the anti–HIV-1 activity of IL-32 was counteracted by M-CSF. Such inhibitory effect of M-CSF was not observed with IL-32–induced M1-like features including high cytokine/chemokine production and strong expression of the costimulatory molecule CD80. However, IL-32–treated macrophages unexpectedly showed also M2-like features including increased phagocytic activity, and high expression of CD14 and the scavenger receptor CD163, and the expression of CD14 and CD163 was further upregulated by cotreatment with M-CSF. The findings of this study regarding the unique functional interplay between M-CSF and IL-32 increase our understanding of the mechanisms that regulate the survival and M1/M2 ratio of macrophages, as well as HIV-1 replication in macrophages.

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Section: Discussionmentioning

confidence: 99%

M-CSF Inhibits Anti–HIV-1 Activity of IL-32, but They Enhance M2-like Phenotypes of Macrophages

Osman

Bhuyan

Hashimoto

et al. 2014

The Journal of Immunology

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“…It is very likely that the observed in vitro differentiation of salmonid mononuclear phagocytes depends on the action of autocrine growth factors, such as the macrophage colony stimulating factor (M-CSF) which is necessary for the development and the differentiation of mononuclear phagocytes to mature macrophages [30]. The action of M-CSF is mediated by ERK [31] and PI3K/Akt-mediated signaling cascades [32]. The gradually increasing levels of p-ERK and p-Akt (a downstream mediator of PI3K signalling) over the course of in vitro incubation correlated with the morphological differentiation of the salmon mononuclear phagocytes and could be explained by the activity of such growth factors.…”

Section: Discussionmentioning

confidence: 99%

CpG- and LPS-activated MAPK signaling in in vitro cultured salmon (Salmo salar) mononuclear phagocytes

Iliev

Hansen

Jørgensen

et al. 2013

Fish & Shellfish Immunology

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“…CSF-1 induces early ( peaking at 5 min) and persistent (starting at 1 h) waves of MEK/Erk1/ 2 phosphorylation. However, only the late wave, which is independent of Grb2/Sos assembly or PI 3-kinase activity, is required for macrophage differentiation (Gobert Gosse et al 2005). Mona, an adaptor protein that increases late Erk1/2 phosphorylation (Bourgin et al 2002) and Gab3 are coinduced during monocytic differentiation in a CSF-1R Tyr-807-dependent manner (Fig.…”

Section: Er Stanley and V Chitumentioning

confidence: 99%

CSF-1 Receptor Signaling in Myeloid Cells

Stanley

Chiţu

2014

Cold Spring Harbor Perspectives in Biology

635

521

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The CSF-1 receptor (CSF-1R) is activated by the homodimeric growth factors colony-stimulating factor-1 (CSF-1) and interleukin-34 (IL-34). It plays important roles in development and in innate immunity by regulating the development of most tissue macrophages and osteoclasts, of Langerhans cells of the skin, of Paneth cells of the small intestine, and of brain microglia. It also regulates the differentiation of neural progenitor cells and controls functions of oocytes and trophoblastic cells in the female reproductive tract. Owing to this broad tissue expression pattern, it plays a central role in neoplastic, inflammatory, and neurological diseases. In this review we summarize the evolution, structure, and regulation of expression of the CSF-1R gene. We discuss the structures of CSF-1, IL-34, and the CSF-1R and the mechanism of ligand binding to and activation of the receptor. We further describe the pathways regulating macrophage survival, proliferation, differentiation, and chemotaxis downstream from the CSF-1R.

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M-CSF stimulated differentiation requires persistent MEK activity and MAPK phosphorylation independent of Grb2–Sos association and phosphatidylinositol 3-kinase activity

Cited by 45 publications

References 42 publications

M-CSF Inhibits Anti–HIV-1 Activity of IL-32, but They Enhance M2-like Phenotypes of Macrophages

M-CSF Inhibits Anti–HIV-1 Activity of IL-32, but They Enhance M2-like Phenotypes of Macrophages

CpG- and LPS-activated MAPK signaling in in vitro cultured salmon (Salmo salar) mononuclear phagocytes

CSF-1 Receptor Signaling in Myeloid Cells

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