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Drosophila PDGF/VEGF signaling from muscles to hepatocyte-like cells protects against obesity

ABSTRACT: Drosophila PDGF/VEGF signaling from muscles to hepatocyte-like cells protects against obesity

PROVIDER: PRJNA615676 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11430248.fastq.gz	Fastqsanger.gz
	SRR11430249.fastq.gz	Fastqsanger.gz
	SRR12601041.fastq.gz	Fastqsanger.gz
	SRR12601042.fastq.gz	Fastqsanger.gz

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Drosophila PDGF/VEGF signaling from muscles to hepatocyte-like cells protects against obesity

Project description:PDGF/VEGF ligands regulate a plethora of biological processes in multicellular organisms via autocrine, paracrine and endocrine mechanisms. Here, we investigated organ-specific roles of Drosophila PDGF/VEGF-like factors (Pvfs). We combine genetic approaches and single-nuclei sequencing to demonstrate that muscle-derived Pvf1 signals to the Drosophila hepatocyte-like cells/oenocytes to suppress lipid synthesis by activating the Pi3K/Akt1/mTOR signaling cascade in the oenocytes. Additionally, we show that this signaling axis regulates the rapid expansion of adipose tissue lipid stores observed in newly eclosed flies. Flies emerge after pupation with limited adipose tissue lipid stores and lipid levels are progressively restored via lipid synthesis. We find that pvf1 expression in the adult muscle increase rapidly during this stage and that muscle-to-oenocyte Pvf1 signaling inhibits restoration of adipose tissue lipid stores as the process reaches completion. Our findings provide the first evidence in a metazoan of a PDGF/VEGF ligand acting as a myokine that regulates systemic lipid homeostasis by activating mTOR in hepatocyte-like cells.

2020-11-09 | GSE147601 | GEO

<i>Drosophila</i> PDGF/VEGF signaling from muscles to hepatocyte-like cells protects against obesity.

Project description:PDGF/VEGF ligands regulate a plethora of biological processes in multicellular organisms via autocrine, paracrine, and endocrine mechanisms. We investigated organ-specific metabolic roles of Drosophila PDGF/VEGF-like factors (Pvfs). We combine genetic approaches and single-nuclei sequencing to demonstrate that muscle-derived Pvf1 signals to the Drosophila hepatocyte-like cells/oenocytes to suppress lipid synthesis by activating the Pi3K/Akt1/TOR signaling cascade in the oenocytes. Functionally, this signaling axis regulates expansion of adipose tissue lipid stores in newly eclosed flies. Flies emerge after pupation with limited adipose tissue lipid stores and lipid level is progressively accumulated via lipid synthesis. We find that adult muscle-specific expression of pvf1 increases rapidly during this stage and that muscle-to-oenocyte Pvf1 signaling inhibits expansion of adipose tissue lipid stores as the process reaches completion. Our findings provide the first evidence in a metazoan of a PDGF/VEGF ligand acting as a myokine that regulates systemic lipid homeostasis by activating TOR in hepatocyte-like cells.

| S-EPMC7752135 | biostudies-literature

Gene based influence of PDGF/VEGF in colorectal cancer

Project description:The aim of the study was to analyse the effects of PDGF and VEGF stimulation on tumor cell proliferation and metabolism for new therapeutic targets in colorectal cancer (CRC).

2018-12-01 | GSE68412 | GEO

Fibroblasts associated with tumors refractory to anti-VEGF treatment

Project description:PDGF-C mediates the angiogenic and tumorigenic properties of fibroblasts associated with tumors refractory to anti-VEGF treatment Tumor associated fibroblasts (TAF) from different tumors exhibit distinct angiogenic and tumorigenic properties. Unlike normal skin fibroblasts (NSF) or TAF (TAF-TIB6) from TIB6 tumors that are sensitive to anti-VEGF treatment, TAF (TAF-EL4) from resistant EL4 tumors can stimulate TIB6 tumor growth even when VEGF is inhibited. We show that platelet-derived growth factor (PDGF)-C is upregulated in TAFs from resistant tumors. PDGF-C neutralizing antibodies blocked the angiogenesis induced by such TAF in vivo and slowed the growth of EL4 and admixture (TAF-EL4 + TIB6) tumors and exhibited additive effects with anti-VEGF-A antibodies. Hence, our data reveal a novel mechanism for TAF mediated tumorigenesis and suggest that some tumors may overcome inhibition of VEGF-mediated angiogenesis through upregulation of PDGF-C

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Analysis of the global gene expression in VEGF-B transgenic rat hearts

Project description:We show that an excess of VEGF-B protects the heart via adaptive cardiac hypertrophy and increased coronary arterial reserve, and by inducing a shift from lipid to glucose metabolism. Six VEGF-B overexpressing transgenic hearts were compared to six littermate wildtype controls

2013-11-30 | E-GEOD-38454 | biostudies-arrayexpress

Analysis of the global gene expression in the rat hearts transduced with adeno-associated viral vectors coding VEGF-B

Project description:We show that an excess of VEGF-B protects the heart via adaptive cardiac hypertrophy and increased coronary arterial reserve, and by inducing a shift from lipid to glucose metabolism. Six hearts transduced with AAV-VEGF-B were compared to six AAV-HSA (human serum albumin) controls

2013-11-30 | E-GEOD-38455 | biostudies-arrayexpress

Analysis of the global gene expression in VEGF-B transgenic rat hearts

2013-11-30 | GSE38454 | GEO

Hepatocyte polyploidization during ageing protects against transcriptional dysregulation and chronic liver disease

Project description:Hepatocyte polyploidization during ageing protects against transcriptional dysregulation and chronic liver disease

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RNA sequencing of HUVECs stimulated with VEGF, OSM+VEGF, or CNTF+CNTFR+VEGF

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Trasncripional regulation by FOXO1 in Vascular Endothelial Cell Growth Factor (VEGF) treatment in human endothelial cells

Project description:FOXO1 was involved in various biologucal processes. In endothelial cells, it has reported that FOXO1 was phosphorylated by PI3K-Akt signaling, and it was nuclear exclusion by short-term VEGF stimulation. This event turns off the expression of apoptosis-related genes, it protects the cell from apoptosis. On the other hand, long-term VEGF stimulation, FOXO1 re-entry into the nucleus and induces the expression of different genes. Therefore, to identify genes regulated by FOXO1 in long-term VEGF stimulation, we performed RNA-seq analysis of FOXO1-knockdowned human unbilical vein endothelial cells (HUVECs) by siRNA and 18h VEGF treatment.

2024-03-01 | GSE220504 | GEO

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