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Macrophage-secreted CSF1 transmits a calorie restriction self-renewing signal to mammary epithelial stem cells

ABSTRACT: Macrophage-secreted CSF1 transmits a calorie restriction self-renewing signal to mammary epithelial stem cells

PROVIDER: PRJNA855904 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20018659_1.fastq.gz	Fastqsanger.gz
	SRR20018659_2.fastq.gz	Fastqsanger.gz
	SRR20018660_1.fastq.gz	Fastqsanger.gz
	SRR20018660_2.fastq.gz	Fastqsanger.gz
	SRR20018661_1.fastq.gz	Fastqsanger.gz

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Macrophage-secreted CSF1 transmits a calorie restriction self-renewing signal to mammary epithelial stem cells

Project description:Calorie restriction (CR) enhances stem cell self-renewal in various tissues, including the mammary gland. The hypothesis propelling this study states that similarly to their intestinal counterparts, mammary epithelial stem cells are insulated from sensing changes in the energy supply and, for that matter, depend on signals from a specific niche. Combined in vivo, in vitro and in silico studies identified macrophages and secreted CSF1 as the energy sensor and paracrine transmitter, respectively, of the CR inducing effect on mammary stem cell self-renewal.

2022-09-28 | GSE207481 | GEO

Macrophage-Secreted CSF1 Transmits a Calorie Restriction-Induced Self-Renewal Signal to Mammary Epithelial Stem Cells.

Project description:Calorie restriction enhances stem cell self-renewal in various tissues, including the mammary gland. We hypothesized that similar to their intestinal counterparts, mammary epithelial stem cells are insulated from sensing changes in energy supply, depending instead on niche signaling. The latter was investigated by subjecting cultures of mammary epithelial stem cells for 8 days to in vivo paracrine calorie-restriction signals collected from a 4-day-conditioned medium of individual mammary cell populations. Conditioned medium from calorie-restricted non-epithelial cells induced latent cell propagation and mammosphere formation-established markers of stem cell self-renewal. Combined RNA-Seq, immunohistochemistry and immunofluorescence analyses of the non-epithelial population identified macrophages and secreted CSF1 as the energy sensor and paracrine signal, respectively. Calorie restriction-induced pStat6 expression in macrophages suggested that skewing to the M2 phenotype contributes to the sensing mechanism. Enhancing CSF1 signaling with recombinant protein and interrupting the interaction with its highly expressed receptor in the epithelial stem cells by neutralizing antibodies were both affected stem cell self-renewal. In conclusion, combined in vivo, in vitro and in silico studies identified macrophages and secreted CSF1 as the energy sensor and paracrine transmitter, respectively, of the calorie restriction-induced effect on mammary stem cell self-renewal.

| S-EPMC9496835 | biostudies-literature

Calorie restriction and aging

Project description:Gene expression profiles of kidney tissue from control-fed 5-month-old, control-fed 30-month-old and calorie restricted 30 month-old C57BL/6 mice. Keywords = kidney, aging, calorie restriction Keywords: other

2003-06-23 | GSE459 | GEO

Comparison between calorie-restricted and time-restricted without calorie restriction

Project description:Comparison between calorie-restricted and time-restricted without calorie restriction

| PRJNA706697 | ENA

G-CSF1

Project description:G-CSF1

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G-CSF1

Project description:G-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.

2024-01-01 | E-MTAB-8088 | biostudies-arrayexpress

Impact of graded calorie restriction on mouse liver protein expression

Project description:Calorie restriction (CR) extends lifespan by modulating the mechanisms involved in aging. We quantified the hepatic proteome of male C57BL/6 mice exposed to graded levels of CR (0% to 40% CR) for three months, and evaluated which signaling pathways were most affected.

2023-10-24 | PXD033436 | Pride

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.

2024-01-01 | E-MTAB-5752 | biostudies-arrayexpress

DPPIV+ fibro-adipogenic progenitors form the niche of adult skeletal muscle self-renewing resident macrophages

Project description:Depending on the tissue, adult tissue-resident macrophages (RMs) are either maintained by blood monocytes or through self-renewal at steady state. While the presence of a nurturing-niche is likely crucial to support the survival and function of self-renewing RMs, evidence regarding its nature is limited. Here, we aimed to characterize the niche for skeletal muscle RMs. We found stromal cells called Fibro-Adipogenic Progenitors (FAPs) to be the main source of colony-stimulating factor 1 (CSF1) in resting skeletal muscle. By utilizing parabiosis in combination with transgenic lines that deplete FAPs (PdgfrαCreERT2 ´ DTA) or conditionally delete FAP-derived CSF1 (PdgfrαCreERT2 ´ Csf1flox/null), we showed that local CSF1 from FAPs is required for the survival of both TIM4- monocyte-derived and TIM4+ self-renewing RMs at steady state in adult skeletal muscle. Following pharmacological depletion of RMs, local CSF1 increases significantly to facilitate their replenishment. Indeed, TIM4- RMs get replaced by blood monocytes following depletion and their numbers increase significantly beyond the normal levels. While a noticeable fraction of TIM4+ RMs also gets replaced by blood monocytes following depletion, their numbers are tightly controlled, which indicates the presence of regulatory mechanisms exclusive to TIM4+ cells. The spatial distribution and number of TIM4+ RMs match with a subpopulation of Dipeptidyl peptidase IV (DPPIV)+ FAPs, suggesting their role as nurturing CSF1-producing niche cells for self-renewing RMs. This finding offers novel opportunities to precisely manipulate the function of self-renewing RMs in situ to further unravel their role in health and disease.

2023-10-24 | GSE241832 | GEO

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