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The effect of a novel form of macrophage colony-stimulating factor (CSF1-Fc) on gene expression in the liver.

ABSTRACT: Treatment of mice with daily injections of CSF1-Fc produce a 50% increase in the size of the liver within 5 days. There was extensive proliferation of hepatocytes, similar to that seen following partial hepatectomy.

ORGANISM(S): Mus musculus

PROVIDER: GSE52636 | GEO | 2013/12/31

SECONDARY ACCESSION(S): PRJNA229512

REPOSITORIES: GEO

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The effect of a novel form of macrophage colony-stimulating factor (CSF1-Fc) on gene expression in the liver.

Project description:Treatment of mice with daily injections of CSF1-Fc produce a 50% increase in the size of the liver within 5 days. There was extensive proliferation of hepatocytes, similar to that seen following partial hepatectomy. Comparative gene expression profiles of the treated and control livers, alongside macrophages grown in CSF1, indicate extensive infiltration by macrophages in response to CSF1-Fc, and demonstrate that infiltrating macrophages produced several candidate mediators of hepatocyte proliferation.

2013-12-31 | E-GEOD-52636 | biostudies-arrayexpress

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Project description:Signalling via the colony stimulating factor 1 receptor (CSF1R) controls the survival, differentiation and proliferation of macrophages which are a source of the somatic growth factor insulin growth factor 1 (IGF1). Treatment of newborn mice with CSF1 has previously been shown to produce an increase in somatic growth rate and we hypothesised that treatment of neonatal low birth weight (LBW) rats with CSF1 would do the same. Growth rates were not affected, yet CSF1 treatment caused an unexpectedly large, but reversible increase in liver size and hepatic fat deposition in both normal and LBW rats. By transcriptional profiling, we have highlighted numerous CSF1-regulated genes known to be involved in lipid droplet formation in the liver and novel candidate genes for further investigation. In contrast to mice and weaner pigs, CSF1 treatment did not increase hepatocyte proliferation in neonatal rats, rather the data were consistent with increased macrophage proliferation instead. This suggests that Kupffer cells promote lipid accumulation in neonates and treatment to ablate CSF1R signalling may reverse lipid accumulation in the liver. Conclusion: Treatment of neonatal rats with CSF1 caused an increase in liver size and hepatic lipid accumulation, due to Kupffer cell expansion and/or activation rather than hepatocyte proliferation Livers were harvested from neonatal rats on Day 6, following 5 days treatment with 1 ug/g porcine CSF1-Fc or PBS by subcutaneous injection. Bone marrow derived macrophages were generated in vitro by culture in CSF1.

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RNAseq of untreated and CSF1-treated, CSF1+QVD-treated monocytes

Project description:Caspases, which are key effectors of apoptosis, have demonstrated non-apoptotic functions. One of these functions is the differentiation into macrophages of peripheral blood monocytes exposed to Colony-Stimulating Factor-1 (CSF1). Macrophage polarization plays an important role in the pathogenesis of diverse human diseases as cancer, leading us to explore if caspase inhibition would affect macrophage polarization. To explore the role of caspases in CSF1 differentiation, we used human monocytes sorted from buffy coats treated by cytokines. We reported that caspase inhibition delays the ex vivo differentiation of peripheral blood monocytes exposed to CSF1 and modifies the phenotype of generated macrophages, e.g. cell shape, surface markers. Moreover, by RNAseq, we observed that the macrophages generated in presence of CSF1 and QVD are different from CSF1-treated monocytes. This study confirms the importance of caspase activation in CSF1 differentiation.

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Liver from CSF1-Fc- or PBS-treated neonatal rats and rat bone marrow derived macrophages

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RNAseq of untreated, CSF1-treated, CSF1+QVD-treated, and GM-CSF-treated monocytes

Project description:Caspases, which are key effectors of apoptosis, have demonstrated non-apoptotic functions. One of these functions is the differentiation into macrophages of peripheral blood monocytes exposed to Colony-Stimulating Factor-1 (CSF1). Conversely, GM-CSF induces the differentiation of monocytes into macrophages in a caspase-independent manner. Macrophages generated by CSF1 and GM-CSF have distinct polarity. Macrophage polarization plays an important role in the pathogenesis of diverse human diseases as cancer, leading us to explore if caspase inhibition would affect macrophage polarization. To explore the role of caspases in CSF1 differentiation, we used human monocytes sorted from buffy coats treated by cytokines. We reported that caspase inhibition delays the ex vivo differentiation of peripheral blood monocytes exposed to CSF1 and modifies the phenotype of generated macrophages, e.g. cell shape, surface markers. Moreover, by RNAseq, we observed that the macrophages generated in presence of CSF1 and QVD are different from CSF1-treated monocytes and from GM-CSF-treated monocytes. Cell cycle and focal adhesion-related pathway genes were selectively down-regulated. This study confirms the importance of caspase activation in CSF1 differentiation.

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Macrophage Colony Stimulating Factor derived from CD4+ T cells aids in control of an intracellular infection [RNA-seq]

Project description:Background: In malaria, parasites of the genus Plasmodium elicit robust host expansion of macrophages and monocytes, but the underlying mechanisms remain unclear. In a microarray analysis of pooled, activated CD4+ T cells from mice infected with P. chabaudi, we detected inducible expression of Csf1, which promotes macrophage proliferation. To better characterize Csf1-producing T cells, single-cell RNA-Seq was performed. Results: Robust Csf1 expression was detected in a subset of sampled CD4+ T cells (n = 14/35), whereas the remainder of cells had no detectable Csf1. Further, we identified ~ 400 genes that were differentially expressed between Csf1+ and Csf1- T cells. Conclusions: This work defines the transcriptional landscape of a subset of activated CD4+ T cells that produce the cytokine Csf1. These cells are expected to be important in infections with intracellular pathogens such as Plasmodium.

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