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Mitochondrial Membrane Potential Regulates Nuclear Gene Expression in Macrophages Exposed to PGE2 (RNA-seq)

ABSTRACT: Mitochondrial Membrane Potential Regulates Nuclear Gene Expression in Macrophages Exposed to PGE2 (RNA-seq)

PROVIDER: PRJNA489441 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7789040_1.fastq.gz	Fastqsanger.gz
	SRR7789040_2.fastq.gz	Fastqsanger.gz
	SRR7789050_1.fastq.gz	Fastqsanger.gz
	SRR7789050_2.fastq.gz	Fastqsanger.gz
	SRR7789060_1.fastq.gz	Fastqsanger.gz

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Mitochondrial Membrane Potential Regulates Nuclear Gene Expression in Macrophages Exposed to PGE2

Project description:Mitochondrial Membrane Potential Regulates Nuclear Gene Expression in Macrophages Exposed to PGE2

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Mitochondrial Membrane Potential Regulates Nuclear Gene Expression in Macrophages Exposed to PGE2 (RNA-seq)

Project description:Metabolic engagement is intrinsic to immune cell function. Prostaglandin E2 (PGE2) has been shown to modulate macrophage activation, yet how PGE2 might affect metabolism is unclear. Here we show that PGE2 causes mitochondrial membrane potential (Δψm) to dissipate in interleukin-4 activated macrophages (M(IL-4)). Effects on Δψm are a consequence of PGE2-initiated transcriptional regulation of genes in the malate-aspartate shuttle (MAS), particularly GOT1. Reduced Δψm causes alterations in the expression of 126 voltage regulated genes (VRGs) including Resistin like molecule-α (RELMα), a key marker of M(IL-4), and genes that regulate cell cycle. The transcription factor ETS variant 1 (ETV1) plays a role in the regulation of 38% of the VRGs. These results reveal ETV1 as a Δψm-sensitive transcription factor, and Δψm as a mediator of mitochondrial-directed nuclear gene expression.

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Mitochondrial Membrane Potential Regulates Nuclear Gene Expression in Macrophages Exposed to PGE2 (ATAC-seq)

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Mitochondrial Membrane Potential Regulates Nuclear Gene Expression in Macrophages Exposed to PGE2

Project description:Metabolic engagement is intrinsic to immune cell function. Prostaglandin E2 (PGE2) has been shown to modulate macrophage activation, yet how PGE2 might affect metabolism is unclear. Here we show that PGE2 causes mitochondrial membrane potential (Δψm) to dissipate in interleukin-4 activated macrophages (M(IL-4)). Effects on Δψm are a consequence of PGE2-initiated transcriptional regulation of genes in the malate-aspartate shuttle (MAS), particularly GOT1. Reduced Δψm causes alterations in the expression of 126 voltage regulated genes (VRGs) including Resistin like molecule-α (RELMα), a key marker of M(IL-4), and genes that regulate cell cycle, The transcription factor ETS variant 1 (ETV1) plays a role in the regulation of 38% of the VRGs. These results reveal ETV1 as a Δψm-sensitive transcription factor, and Δψm as a mediator of mitochondrial-directed nuclear gene expression.

2021-09-08 | PXD010997 | Pride

Mitochondrial Membrane Potential Regulates Nuclear Gene Expression in Macrophages Exposed to PGE2 (ATAC-seq)

Project description:Mitochondrial Membrane Potential Regulates Nuclear Gene Expression in Macrophages Exposed to PGE2 (ATAC-seq)

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Mitochondrial Membrane Potential Regulates Nuclear Gene Expression in Macrophages Exposed to PGE2

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-01-16 | GSE119521 | GEO

Mitochondrial Membrane Potential Regulates Nuclear Gene Expression in Macrophages Exposed to Prostaglandin E2.

Project description:Metabolic engagement is intrinsic to immune cell function. Prostaglandin E2 (PGE2) has been shown to modulate macrophage activation, yet how PGE2 might affect metabolism is unclear. Here, we show that PGE2 caused mitochondrial membrane potential (Δψm) to dissipate in interleukin-4-activated (M(IL-4)) macrophages. Effects on Δψm were a consequence of PGE2-initiated transcriptional regulation of genes, particularly Got1, in the malate-aspartate shuttle (MAS). Reduced Δψm caused alterations in the expression of 126 voltage-regulated genes (VRGs), including those encoding resistin-like molecule α (RELMα), a key marker of M(IL-4) cells, and genes that regulate the cell cycle. The transcription factor ETS variant 1 (ETV1) played a role in the regulation of 38% of the VRGs. These results reveal ETV1 as a Δψm-sensitive transcription factor and Δψm as a mediator of mitochondrial-directed nuclear gene expression.

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