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Progressive accumulation of resting cells ensures the lifelong maintenance of the hippocampal stem cell population

ABSTRACT: Progressive accumulation of resting cells ensures the lifelong maintenance of the hippocampal stem cell population

PROVIDER: PRJNA670445 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12859900.fastq.gz	Fastqsanger.gz
	SRR12859901.fastq.gz	Fastqsanger.gz
	SRR12859902.fastq.gz	Fastqsanger.gz
	SRR12859903.fastq.gz	Fastqsanger.gz
	SRR12859904.fastq.gz	Fastqsanger.gz

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Progressive accumulation of resting cells ensures the lifelong maintenance of the hippocampal stem cell population

Project description:Neural stem cell numbers fall rapidly in the hippocampus of juvenile mice but stabilise during adulthood, ensuring lifelong hippocampal neurogenesis. We show that this reduction in stem cell depletion rate in young adults is the result of coordinated changes in stem cell behaviour. In particular, while proliferating neural stem cells in juveniles differentiate rapidly, they increasingly return to a resting state of shallow quiescence and progress through additional self-renewing divisions in adulthood. Single-cell transcriptomic, modelling and label-retention analyses indicate that resting cells have a higher activation rate and greater contribution to neurogenesis than dormant cells, which have not left quiescence. These progressive changes in stem cell behaviour result from reduced expression of the pro-activation protein ASCL1 due to increased post-translational degradation. These cellular mechanisms help reconcile current contradictory models of hippocampal NSC dynamics and may contribute to the different rates of decline of hippocampal neurogenesis in mammalian species including humans.

2020-12-15 | GSE159768 | GEO

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Expression profiling of Human Muscle-Derived RNAs within the study Lifelong Football Training: effects on autophagy and healthy longevity promotion

Project description:Aging is a physiological process characterized by a progressive decline of biological functions and an increase in destructive processes in cells and organs. Physical activity and exercise positively affects the expression of skeletal muscle markers involved in longevity pathways. Recently, a new mechanism, autophagy, was introduced to the adaptations induced by acute and chronic exercise as responsible of positive metabolic modification and health-longevity promotion. However, the molecular mechanisms regulating autophagy in response to physical activity and exercise are sparsely described. We investigated the long-term adaptations resulting from lifelong recreational football training on the expression of skeletal muscle markers involved in autophagy signaling. We demonstrated that lifelong football training increased the expression of messengers: RAD23A, HSPB6, RAB1B, TRAP1, SIRT2 and HSBPB1, involved in the auto-lysosomal and proteasome-mediated protein degradation machinery; of RPL1, RPL4, RPL36, MRLP37, involved in cellular growth and differentiation processes; of the Bcl-2, HSP70, HSP90, PSMD13 and of the ATG5-ATG12 protein complex, involved in proteasome promotion and autophagy processes in muscle samples from lifelong trained subjects compared to age-matched untrained controls. In conclusion, our results indicated that lifelong football training positively influence exercise-induced autophagy processes and protein quality control in skeletal muscle, thus promoting healthy aging. The aim of the present research was to investigate, through a differential transcriptomic approach, the effects of lifelong recreational football training on the expression of key markers involved in the autophagy response for the maintenance of protein quality control, related to healthy longevity promotion, in skeletal muscle from VPG compared to elderly untrained control subjects.

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Lifelong calorie restriction and markers of colonic health in aging mice

Project description:Diminishment of colonic health is associated with various age-related pathologies. Calorie restriction (CR) is an efficient strategy to increase healthy lifespan, although underlying mechanisms are not fully elucidated. Here we report the effects of lifelong CR on markers of colonic health in aging mice. We show that 30% energy reduction, as compared to a control (C) and moderate-fat (MF) diet, is associated with attenuated immune-related gene expression and lower levels of bile acids in the colon. Pronounced shifts in microbiota composition, together with lowered plasma levels of interleukin 6, in mice exposed to CR are in line with these findings. Furthermore, expression of genes involved in lipid metabolism was higher upon CR as compared to C and MF, pointing towards efficient regulation of energy metabolism. Switching from CR to an ad libitum MF diet at old age revealed remarkable phenotypic plasticity, although expression of a small subset of genes remained CR-associated. This research demonstrates that CR beneficially affects markers of colonic health in aging mice and as such may attenuate the progressive age-related decline in health.

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Ovine progressive pneumonia virus

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Rapid accumulation of motility-activating mutations in resting liquid culture of Escherichia coli

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Loss of NAD homeostasis leads to progressive and reversible degeneration of skeletal muscle

Project description:NAD is an obligate co-factor for the catabolism of metabolic fuels in all cell types. However, the availability of NAD in several tissues can become limited during genotoxic stress and the course of natural aging. The point at which NAD restriction imposes functional limitations on tissue physiology remains unknown. We examined this question in murine skeletal muscle by specifically depleting Nampt, an essential enzyme in the NAD salvage pathway. Knockout mice exhibited a dramatic 85% decline in intramuscular NAD content, accompanied by fiber degeneration and progressive loss of both muscle strength and treadmill endurance. Administration of the NAD precursor nicotinamide riboside rapidly ameliorated functional deficits and restored muscle mass, despite having only a modest effect on the intramuscular NAD pool. Additionally, lifelong overexpression of Nampt preserved muscle NAD levels and exercise capacity in aged mice, supporting a critical role for tissue-autonomous NAD homeostasis in maintaining muscle mass and function. Messenger RNA was isolated from quadriceps muscle of mice from three different age groups and three different genotypes. Wildtype mice were aged 4, 7, and 24 months. Mice deficient for Nampt in skeletal muscle (mNKO) were aged 7 months. Mice overexpressing Nampt in skeletal muscle were aged 4 and 24 months.

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