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Lifelong dietary protein restriction accelerates skeletal muscle loss and reduces muscle fibre size by impairing proteostasis and mitochondrial homeostasis

ABSTRACT: Lifelong dietary protein restriction accelerates skeletal muscle loss and reduces muscle fibre size by impairing proteostasis and mitochondrial homeostasis

PROVIDER: PRJNA987566 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25032436_1.fastq.gz	Fastqsanger.gz
	SRR25032436_2.fastq.gz	Fastqsanger.gz
	SRR25032437_1.fastq.gz	Fastqsanger.gz
	SRR25032437_2.fastq.gz	Fastqsanger.gz
	SRR25032438_1.fastq.gz	Fastqsanger.gz

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Lifelong dietary protein restriction accelerates skeletal muscle loss and reduces muscle fibre size by impairing proteostasis and mitochondrial homeostasis.

Project description:The early life environment significantly affects the development of age-related skeletal muscle disorders. However, the long-term effects of lactational protein restriction on skeletal muscle are still poorly defined. Our study revealed that male mice nursed by dams fed a low-protein diet during lactation exhibited skeletal muscle growth restriction. This was associated with a dysregulation in the expression levels of genes related to the ribosome, mitochondria and skeletal muscle development. We reported that lifelong protein restriction accelerated loss of type-IIa muscle fibres and reduced muscle fibre size by impairing mitochondrial homeostasis and proteostasis at 18 months of age. However, feeding a normal-protein diet following lactational protein restriction prevented accelerated fibre loss and fibre size reduction in later life. These findings provide novel insight into the mechanisms by which lactational protein restriction hinders skeletal muscle growth and includes evidence that lifelong dietary protein restriction accelerated skeletal muscle loss in later life.

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Lifelong dietary protein restriction accelerates skeletal muscle loss and reduces muscle fibre size by impairing proteostasis and mitochondrial homeostasis

Project description:To reveal the possible underlying mechanisms of protein restriction during lactation, we compared the transcriptomic profiles of GAS muscles from 21-day-old offsrping from mothers on a low protein diet during lactation and control group using RNAseq analysis.

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Cotton Fibre/Non Fibre

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Cotton Fibre/Non Fibre

Project description:0dpa Fibre vs epidermal laser capture microdisection comparison Total RNA was isolated from each cell type (fibre initial or non-fibre epidermal pavement cell) from both Plant 1 and Plant 2. Hence, there were two biological replicates of each cell-type. Sub-samples of each cell type, designated here as technical replicates, were taken as separate batches of cells from different groups of ovules, but each from the same pair of plants. In particular, there were four sub-samples of fibre initial cells from plant 1 and two from plant 2 and two sub-samples of non-fibre epidermal from plant 1 and four from plant 2. The complete experiment involved three dye-swap pairs using a total of 6 arrays.

2006-06-26 | E-GEOD-5133 | biostudies-arrayexpress

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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Radiation-induced damage to prepubertal Pax7+ skeletal muscle stem cells drives lifelong deficits in myofiber size and nuclear number

Project description:During prepubertal development, muscle stem cells (satellite cells, SCs) actively contribute to myofiber growth. Because some SCs are active during this time, they may be particularly susceptible to damage. Using a Small Animal Radiation Research Platform (SARRP), we investigated the effects of local fractionated radiation treatment on prepubertal SCs. Immediately after this regimen, there was a reduction in SC number. Although surviving SCs had deficiencies in function, some myogenic potential remained. Indeed, some muscle regenerative capacity persisted immediately after irradiation. Lastly, we assessed the long-term consequences of radiation-induced SC loss during prepuberty. We observed a reduction of myofiber size and corresponding loss of nuclei in both fast- and slow-contracting muscles 14 months post-irradiation. Notably, prepubertal SC depletion mimicked these lifelong deficits. This work highlights the susceptibility of prepubertal SCs to radiation exposure. We also reveal the importance of prepubertal SC contribution to the lifelong maintenance of skeletal muscle.

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Small molecule proteostasis regulators that reprogram the ER to reduce extracellular protein aggregation

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