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Effect of aging on mitochondrial gene expression using C57BL/6N liver mitochondria

ABSTRACT: Effect of aging on mitochondrial gene expression using C57BL/6N liver mitochondria

PROVIDER: PRJNA858664 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20187062_1.fastq.gz	Fastqsanger.gz
	SRR20187063_1.fastq.gz	Fastqsanger.gz
	SRR20187064_1.fastq.gz	Fastqsanger.gz
	SRR20187065_1.fastq.gz	Fastqsanger.gz
	SRR20187066_1.fastq.gz	Fastqsanger.gz

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Effect of aging on mitochondrial gene expression using C57BL/6N liver mitochondria

Project description:To investigate the effect of aging on mitochondrial gene expression we isolated liver mitochondria from 4 12-week and 4 65-week C57BL/6N WT mice. We then isolated RNA and prepared the barcoded library using PCR-cDNA Barcoding Kit SQK-PCB109 and ran it on MinIOn R9.4.1 Flow cells.

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Project description:ER stress could affect many tissues, especially liver, in which non-alcoholic fatty liver disease, liver steatosis, etc. have been reported relative. But there still lack systematic insight into ER stress in liver, which can be obtained by transcriptomics of the tissue. Here, tunicamycin was utilized to induce ER stress in C57BL/6N mice. And microarray was performed to get the transcriptome alteration. Microarray of liver from tunicamycin-injected C57Bl/6N mice

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Project description:Aging is the progressive decline in organismal function that leads to an increased risk of multiple diseases and mortality. The molecular basis of this decline is unknown. Using quantitative PCR for mitochondrial mRNA from multiple tissues from the same animals, we found that the rate of change in mouse mitochondrial expression is tissue-specific, with cardiac expression declining early (8-10 months), adipose expression declining late (25-30 months), and no change in kidney or skin. In cardiac tissue, mitochondria-derived mRNA levels declined more slowly than nuclear encoded mRNAs, suggesting a potential dysregulation. These changes were independent of alteration in mitochondrial number, as measured by quantitative PCR of mitochondrial DNA and citrate synthase activity. We found no change in the variability between mitochondrial mRNA levels with age, suggesting that the changes are not due to random dysregulation at the level of gene expression. Caloric restriction (CR), a lifespan-extending intervention proposed to act through mitochondrial biogenesis, delayed the decline in both cardiac and adipose mitochondrial mRNA levels of F344 rats. CR caused an increase in citrate synthase activity but did not alter mitochondrial DNA content, indicating increased translation or reduced turnover of mitochondrial proteins. These results demonstrate that mitochondrial gene expression changes with age are not coupled to mitochondrial number, are likely to be regulated, and are governed by tissue-specific processes. These findings indicate that aging is neither a programmed organism-wide change orchestrated in a top-down fashion nor a product of random dysregulation of gene expression but that tissue-specific factors may independently control aging in different organ compartments. Keywords: aging Cardiac ventricle total RNA from 10 young (4-6 month) and 10 young (25-28 month) mice were compared.

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Mus musculus strain:C57Bl/6N

Project description:Mus musculus strain:C57Bl/6N Raw sequence reads

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Mus musculus strain:C57Bl/6N

Project description:Mus musculus strain:C57Bl/6N Raw sequence reads

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Mus musculus cultivar:C57BL/6N

Project description:Mus musculus cultivar:C57BL/6N Raw sequence reads

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Mus musculus strain:C57BL/6N

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STAT3 Modulates CD4+ T Mitochondrial Dynamics and Function in Aging

Project description:Aging promotes numerous intracellular changes in T cells that impact their effector function. Our data shows that aging promotes an increase in localization of STAT3 to the mitochondria (mitoSTAT3), which promotes changes in mitochondrial dynamics and function and has a mechanistic link to T cell cytokine production. More specifically, mitoSTAT3 increased activity of aging T cell mitochondria due to STAT3’s effect on complex II. Limiting mitoSTAT3 using a mitochondria targeted curcuminoid, Mtcur-1, lowered complex II activity, prevented age-induced changes in mitochondrial dynamics and function, and reduced proinflammatory Th17 inflammation. Exogenous expression of the constitutively phosphorylated form of STAT3 in T cells from young adults mimicked changes in mitochondrial dynamics and function in T cells from older adults and partially recapitulated aging-induced cytokine profiles. Our data shows the mechanistic link among mitoSTAT3, mitochondrial dynamics,function and T cell cytokine production.

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