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Genomic instability in the naturally and prematurely aged myocardium

ABSTRACT: Genomic instability in the naturally and prematurely aged myocardium

PROVIDER: PRJNA510744 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8352390_1.fastq.gz	Fastqsanger.gz
	SRR8352390_2.fastq.gz	Fastqsanger.gz
	SRR8352400_1.fastq.gz	Fastqsanger.gz
	SRR8352400_2.fastq.gz	Fastqsanger.gz
	SRR8352410_1.fastq.gz	Fastqsanger.gz

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Genomic instability in the naturally and prematurely aged myocardium [RNA-Seq]

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Genomic instability in the naturally and prematurely aged myocardium [variants: data set 1]

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Genomic instability in the naturally and prematurely aged myocardium [RNA-Seq]

Project description:Our data demonstrate that genomic instability does not evidently contribute to naturally aging of the mouse heart and support the contention that the endogenous DNA repair machinery is remarkably active to maintain genomic integrity in cardiac cells throughout life.

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Genomic instability in the naturally and prematurely aged myocardium.

Project description:Genomic instability, the unresolved accumulation of DNA variants, is hypothesized as one of the contributors to the natural aging process. We assessed the frequency of unresolved DNA damage reaching the transcriptome of the murine myocardium during the course of natural aging and in hearts from four distinct mouse models of premature aging with established aging-related cardiac dysfunctions. RNA sequencing and variant calling based on total RNA sequencing was compared between hearts from naturally aging mice, mice with cardiomyocyte-specific deficiency of Ercc1, a component of the DNA repair machinery, mice with reduced mitochondrial antioxidant capacity, Tert-deficient mice with reduced telomere length, and a mouse model of human Hutchinson-Gilford progeria syndrome (HGPS). Our results demonstrate that no enrichment in variants is evident in the naturally aging murine hearts until 2 y of age from the HGPS mouse model or mice with reduced telomere lengths. In contrast, a dramatic accumulation of variants was evident in Ercc1 cardiomyocyte-specific knockout mice with deficient DNA repair machinery, in mice with reduced mitochondrial antioxidant capacity, and in the intestine, liver, and lung of naturally aging mice. Our data demonstrate that genomic instability does not evidently contribute to naturally aging of the mouse heart in contrast to other organs and support the contention that the endogenous DNA repair machinery is remarkably active to maintain genomic integrity in cardiac cells throughout life.

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Genomic instability in the naturally and prematurely aged myocardium

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

2021-09-15 | GSE124087 | GEO

Theophylline derivatives promote the activation of primordial follicles and ameliorate fertility deficits in naturally aged mice

Project description:The residual dormant primordial follicles in aged women and patients with premature ovarian insufficiency (POI) are difficult to activate in vivo. In this study, we found that PDE1A, PDE2A and PDE6D were expressed mainly in mouse primordial follicle oocytes and that PDE1A and PDE2A levels were significantly decreased during the activation of primordial follicles. The specific inhibitors of PDE1 (nimodipine), PDE2 (EHNA) and PDE5/6 (zaprinast) and the nonspecific PDE inhibitors theophylline derivatives (including aminophylline, dyphylline, enprofylline, choline theophyllinate, doxofylline, arofylline and lisofylline) activated mouse primordial follicles. These inhibitors also increased the levels of cyclic adenosine monophosphate (cAMP) and phosphorylated protein kinase B (p-Akt) in cultured mouse ovaries. Moreover, the administration of aminophylline, dyphylline and enprofylline to neonatal mice by intraperitoneal injection and to adolescent mice by oral treatment increased the number of growing follicle and the levels of p-Akt in the ovaries. Importantly, the oral administration of aminophylline increased the quantity and quality of ovulated oocytes and the number of offspring in naturally aged mice. In addition, aminophylline, dyphylline and enprofylline activated human primordial follicles and increased p-Akt levels. Thus, theophylline derivatives activate primordial follicles by increasing cAMP levels and activating the PI3K/Akt pathway, and the oral administration of aminophylline increases fertility in naturally aged female mice. As oral medications, theophylline derivatives may be used to increase fertility in aged women and patients with POI.

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Naturally-aged microglia exhibit phagocytic dysfunction accompanied by gene expression changes reflective of underlying neurologic disease

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