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Mitochondrial Calcium Exchange links Metabolism with the Epigenome to Control Cellular Differentiation (RNA-seq)

ABSTRACT: Mitochondrial Calcium Exchange links Metabolism with the Epigenome to Control Cellular Differentiation (RNA-seq)

PROVIDER: PRJNA559174 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9920780.fastq.gz	Fastqsanger.gz
	SRR9920790.fastq.gz	Fastqsanger.gz
	SRR9920781.fastq.gz	Fastqsanger.gz
	SRR9920791.fastq.gz	Fastqsanger.gz
	SRR9920782.fastq.gz	Fastqsanger.gz

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Mitochondrial Calcium Exchange links Metabolism with the Epigenome to Control Cellular Differentiation

Project description:Mitochondrial Calcium Exchange links Metabolism with the Epigenome to Control Cellular Differentiation

| PRJNA559172 | ENA

Mitochondrial Calcium Exchange links Metabolism with the Epigenome to Control Cellular Differentiation (ATAC-seq)

Project description:Mitochondrial Calcium Exchange links Metabolism with the Epigenome to Control Cellular Differentiation (ATAC-seq)

| PRJNA559175 | ENA

Mitochondrial Calcium Exchange links Metabolism with the Epigenome to Control Cellular Differentiation (ATAC-seq)

Project description:Fibroblast to myofibroblast differentiation is crucial for the initial healing response but excessive myofibroblast activation leads to pathological fibrosis. Therefore, it is imperative to understand the mechanisms underlying myofibroblast formation. Here we report that mitochondrial calcium (mCa2+) signaling is a regulatory mechanism in myofibroblast differentiation and fibrosis. We demonstrate that inhibition of mCa2+ uptake in fibroblasts enhances myofibroblast formation and this translates to increased fibrosis following injury. Fibrotic signaling alters the gating of the mitochondrial calcium uniporter (mtCU) to reduce mCa2+ uptake and induce specific changes in metabolism. mCa2+-dependent metabolic reprogramming leads to the activation of αKG-dependent demethylases which epigenetically modify promoter regions specific to the myofibroblast gene program resulting in differentiation. Our results uncover an important role for mCa2+ uptake beyond metabolic regulation and cell death and demonstrate that mCa2+ signaling regulates the epigenome to influence cellular differentiation.

2019-08-22 | GSE135530 | GEO

Mitochondrial Calcium Exchange links Metabolism with the Epigenome to Control Cellular Differentiation (RNA-seq)

2019-08-22 | GSE135529 | GEO

Mitochondrial calcium exchange links metabolism with the epigenome to control cellular differentiation.

Project description:Fibroblast to myofibroblast differentiation is crucial for the initial healing response but excessive myofibroblast activation leads to pathological fibrosis. Therefore, it is imperative to understand the mechanisms underlying myofibroblast formation. Here we report that mitochondrial calcium (mCa2+) signaling is a regulatory mechanism in myofibroblast differentiation and fibrosis. We demonstrate that fibrotic signaling alters gating of the mitochondrial calcium uniporter (mtCU) in a MICU1-dependent fashion to reduce mCa2+ uptake and induce coordinated changes in metabolism, i.e., increased glycolysis feeding anabolic pathways and glutaminolysis yielding increased α-ketoglutarate (αKG) bioavailability. mCa2+-dependent metabolic reprogramming leads to the activation of αKG-dependent histone demethylases, enhancing chromatin accessibility in loci specific to the myofibroblast gene program, resulting in differentiation. Our results uncover an important role for the mtCU beyond metabolic regulation and cell death and demonstrate that mCa2+ signaling regulates the epigenome to influence cellular differentiation.

| S-EPMC6778142 | biostudies-literature

Mitochondrial Calcium Exchange links Metabolism with the Epigenome to Control Cellular Differentiation

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

2019-08-22 | GSE135531 | GEO

Inositol triphosphate-triggered calcium release blocks lipid exchange at endoplasmic reticulum-Golgi contact sites

Project description:Vesicular traffic and membrane contact sites between organelles enable the exchange of proteins, lipids, and metabolites. Recruitment of membrane tethers to contact sites between the endoplasmic reticulum (ER) and the plasma membrane is often triggered by calcium. In contrast, we reveal here a function for calcium in the repression of cholesterol export at membrane contact sites between the ER and the Golgi complex. We show that calcium efflux from ER stores induced by inositol-triphosphate [IP3] accumulation upon loss of the inositol 5-phosphatase INPP5A or sustained receptor signaling triggers the depletion of cholesterol and associated complex glycosphingolipids from the cell surface, resulting in a blockade of clathrin-independent endocytosis (CIE) of bacterial Shiga toxin. This phenotype is caused by the calcium-induced dissociation of oxysterol binding protein (OSBP) from the Golgi complex and from VAP-containing membrane contact sites. Our findings reveal a crucial function for INPP5A-mediated IP3 hydrolysis in the control of lipid exchange at membrane contact sites.

2021-05-06 | MTBLS2444 | MetaboLights

TRPC1 links calcium signaling to cellular senescence in the protection against post-traumatic osteoarthritis

Project description:TRPC1 links calcium signaling to cellular senescence in the protection against post-traumatic osteoarthritis

| PRJNA1216926 | ENA

Mitochondrial calcium uniporter links acetyl-CoA metabolism and H3K27 acetylation to maintain glioblastoma stem cells

Project description:Mitochondrial calcium uniporter links acetyl-CoA metabolism and H3K27 acetylation to maintain glioblastoma stem cells

| PRJNA1220592 | ENA

The Mitochondrial Calcium Uniporter controls skeletal muscle mass in vivo

Project description:Muscle atrophy contributes to the poor prognosis of many physiopathological conditions, but pharmacological therapies are still limited. Muscle activity leads to major swings in mitochondrial [Ca2+] which control aerobic metabolism, cell death and survival pathways. We have investigated in vivo the effects of mitochondrial Ca2+ homeostasis in skeletal muscle function and trophism, by overexpressing or silencing the Mitochondrial Calcium Uniporter (MCU). The results coherently demonstrate that both in developing and in adult muscles MCU-dependent mitochondrial Ca2+ uptake has a marked trophic effect that does not depend on autophagy or aerobic control, but impinges on two major hypertrophic pathways of skeletal muscle, PGC-1M-NM-14 and Igf1-Akt/PKB. In adult mice, MCU overexpression protects from denervation-induced atrophy. These data reveal a novel Ca2+-dependent organelle-to-nucleus signaling route, which links mitochondrial function to the control of muscle mass and may represent a possible pharmacological target in sarcopenia. Experiments were performed on biological replicates of single skeletal muscle fibres. Seven fibres were chosen for their Mutochondrial Calcium Uniporter (MCU) overexpression and other seven fibres because MCU was silenced. Overexpression and silencing were performed injecting skeletal muscle with AAV containing MCU gene or short interfering oligos specific for MCU. As control was profiled eigth fibres transfected with AAV and eigth wild type fibres. Analyses were performed 7 days and 14 days after the AAV injection (3 fibers after 7 days and 4 fibers after 14 days for MCU overexpression and silencing, four fibres after 7 days and four after 14 days for control).

2015-03-05 | E-GEOD-60931 | biostudies-arrayexpress

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