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Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health

ABSTRACT: Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health

PROVIDER: PRJNA418766 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6298091_1.fastq.gz	Fastqsanger.gz
	SRR6298091_2.fastq.gz	Fastqsanger.gz
	SRR6298092_1.fastq.gz	Fastqsanger.gz
	SRR6298092_2.fastq.gz	Fastqsanger.gz
	SRR6298093_1.fastq.gz	Fastqsanger.gz

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Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health

Project description:Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health

| PRJNA418943 | ENA

Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health

Project description:The short-lived turquoise killifish Nothobranchius furzeri (Nfu) is a valid model for aging studies. Here, we investigated its age-associated cardiac function. We observed oxidative stress accumulation and an engagement of microRNAs (miRNAs) in the aging heart. MiRNA-sequencing of 5 week (young), 12-21 week (adult) and 28-40 week (old) Nfu hearts revealed 23 up-regulated and 18 down-regulated miRNAs with age. MiR-29 family turned out as one of the most up-regulated miRNAs during aging. MiR-29 family increase induces a decrease of known targets like collagens and DNA methyl transferases (DNMTs) paralleled by 5´methyl-cytosine (5mC) level decrease. To further investigate miR-29 family role in the fish heart we generated a transgenic zebrafish model where miR-29 was knocked-down. In this model we found significant morphological and functional cardiac alterations and an impairment of oxygen dependent pathways by transcriptome analysis leading to hypoxic marker up-regulation. To get insights the possible hypoxic regulation of miR-29 family, we exposed human cardiac fibroblasts to 1% O2 levels. In hypoxic condition we found miR-29 down-modulation responsible for the accumulation of collagens and 5mC. Overall, our data suggest that miR-29 family up-regulation might represent an endogenous mechanism aimed at ameliorating the age-dependent cardiac damage leading to hypertrophy and fibrosis.

2018-02-27 | GSE107003 | GEO

Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health

Project description:Comparison of miRNA expression profiles from male Nothobranchius furzeri (strain MZM-0410) hearts in different age groups. The small-RNA-seq data comprises 3 groups

2018-02-27 | GSE107062 | GEO

Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health.

| S-EPMC5715159 | biostudies-literature

Enteric bacteria increase the defenses against oxidative stress in Entamoeba histolytica

Project description:Enteric bacteria increase the defenses against oxidative stress in Entamoeba histolytica

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Folic Acid study in HT-29 cells

Project description:Low intracellular folate levels diminish the growth rate of HT-29 human colon cancer cells. This is accompanied by a metabolic shift from cytosolic glycolysis towards mitochondrial oxidative phosphorylation, as demonstrated by a lower lactate production and an increased mitochondrial oxygen consumption rate. To obtain insight in the molecular effects underlying these changes, the steady state gene expression profiles of HT-29 cells with different intracellular folate concentrations were compared. The gene expression profile of HT-29 cells with low intracellular folate levels (grown for 3 weeks in 10 ng/ml folic acid (PGA)) was clearly distinct from that of the other exposure conditions, which provide sufficient intracellular folate levels (100 ng/ml PGA, 10 ng/ml methyltetrahydrofolate (MTHF) or 100 ng/ml MTHF). Intracellular folate deficiency, contrary to expectation, did not lead to major changes in expression of genes involved in energy metabolism. This suggests that the shift towards mitochondrial oxidative phosphorylation is not mediated at the transcription level. Furthermore, only minor changes in the expression of folate metabolism related genes were observed. The changes that were observed were consistent with nucleotide salvage and in agreement with nucleotide need of the slow-growing folate-deficient HT-29 cells. The major observed effects were on cell cycle related gene expression, which was increased and interferon-responsive gene expression, which was reduced. The increase in cell cycle related gene expression seems compensatory to the reduced cell growth. Down-regulation of the interferon-response may be explained by decreased expression of signal transducer and activator of transcription 1 upon folate deficiency. Keywords: dose response, folic acid, HT-29 cells, human

2005-08-13 | GSE3099 | GEO

Peroxiredoxin 1 protects telomeres from oxidative damage preserving chromosome ends for extension by telomerase

Project description:With the increase of atmospheric oxygen 2.3 billion years ago, mechanisms evolved to mitigate the toxic effects of oxygen radicals. Telomeres appear particularly susceptible to oxidative damage, which leads to cellular and organismal aging, cancer, cardiac failure and other diseases. Specific mechanisms of telomere protection from oxidative damage and the molecular consequences of the damage have not been described. Here, we identify the antioxidant enzyme peroxiredoxin 1 (PRDX1) enriched in telomeric chromatin in S and G2 phases of the cell cycle during which telomeres become replicated. PRDX1 depletion leads to oxidative damage of telomeric DNA without affecting the bulk of genomic DNA. The oxidized nucleotide 8-oxo-2’deoxyguanosine-5’-triphosphate (8oxodGTP) can be incorporated by telomerase into telomeric repeats but it mediates premature chain termination when incorporated as first G in the telomeric 5’-TTAGGG-3’ sequence. In dependency of the alignment position within the telomerase RNA template, terminus 8oxoG containing DNA substrates also completely block extension by telomerase. We propose two major mechanisms by which PRDX1 counteracts telomere damage and aging. In safeguarding telomeres from oxygen radicals, PRDX1 prevents DNA damage, telomere replication defects and mutations that will perturb recognition of telomeric DNA by shelterin components. In preventing modification of the telomeric DNA substrate and the dNTP pool, PRDX1 preserves telomeres for elongation by telomerase.

2016-12-07 | PXD002626 | Pride

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Project description:Vibrio parahaemolyticus strain:29-1 | isolate:29-1 Genome sequencing and assembly

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Vibrio parahaemolyticus strain:29-2 | isolate:29-2

Project description:Vibrio parahaemolyticus strain:29-2 | isolate:29-2 Genome sequencing and assembly

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Identification of LIN-29 target genes

Project description:To further explore the regulatory network coordinated by LIN-29, and to possibly uncover potential new roles for this transcription factor, we searched for its downstream target genes at the genomic level. To do this, we chose not to modify LIN-29 expression via loss-of-function mutations in upstream heterochronic pathway components, but rather to temporally misexpress LIN-29 directly and examine changes in development and in gene expression.

2021-08-10 | GSE118433 | GEO

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