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

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

PROVIDER: PRJNA559172 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9920780.fastq.gz	Fastqsanger.gz
	SRR9920790.fastq.gz	Fastqsanger.gz
	SRR9920800.fastq.gz	Fastqsanger.gz
	SRR9920810.fastq.gz	Fastqsanger.gz
	SRR9920820.fastq.gz	Fastqsanger.gz

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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 (RNA-seq)

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

| PRJNA559174 | 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

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

Project description:Transient receptor potential channel 1 (TRPC1) is a widely expressed mechanosensitive ion channel located within the endoplasmic reticulum membrane, crucial for refilling depleted internal calcium stores during activation of calcium-dependent signaling pathways. Here, we have demonstrated that TRPC1 activity is protective within cartilage homeostasis in the prevention of cellular senescence associated cartilage breakdown during mechanical and inflammatory challenge. We revealed that TRPC1 loss is associated with early stages of osteoarthritis (OA) and plays a non-redundant role in calcium signaling in chondrocytes. Trpc1-/- mice subjected to destabilization of the medial meniscus induced OA developed a more severe OA phenotype than wild type controls. During early OA development, Trpc1-/- mice displayed an increased chondrocyte survival rate, however remaining cells displayed features of senescence including p16INK4a expression and decreased Sox9. RNA sequencing identified differentially expressed genes related to cell number, apoptosis and extracellular matrix organization. Trpc1-/- chondrocytes exhibited accelerated dedifferentiation, while demonstrating an increased susceptibility to cellular senescence. Targeting the mechanism of TRPC1 activation may be a promising therapeutic strategy in osteoarthritis prevention.

2025-02-10 | GSE288320 | GEO

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