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Circadian mRNA expression in skeletal muscle of young and aged mice

ABSTRACT: Aging animals undergo a variety of changes in molecular processes. Among these, the cellular circadian clock has been shown to change as animals age. Moreover, there is evidence that also core circadian clock proteins could influence the ageing behavior of vertebrates. To investigate the interplay between aging and the circadian clock, we studied circadian mRNA expression in skeletal muscles from young (8 weeks) and aged (80 weeks) mice. In order to detect differences in circadian patterns, we used microarray-based transcriptome-wide time series of mRNA expression, containing 16 independent measurements for both young and aged animals. Each individual time point consists of total RNA from hind limb skeletal muscles from 3 different animals. Young and aged mice where entrained to 12 hr/12 hr light-dark conditions. From these mice, hind limb skeletal muscles were extracted at different times of day, in order to measure circadian mRNA expression patterns.

ORGANISM(S): Mus musculus

SUBMITTER: Paul Thaben

PROVIDER: E-GEOD-75523 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Circadian mRNA expression in skeletal muscle of young and aged mice

Project description:Aging animals undergo a variety of changes in molecular processes. Among these, the cellular circadian clock has been shown to change as animals age. Moreover, there is evidence that also core circadian clock proteins could influence the ageing behavior of vertebrates. To investigate the interplay between aging and the circadian clock, we studied circadian mRNA expression in skeletal muscles from young (8 weeks) and aged (80 weeks) mice. In order to detect differences in circadian patterns, we used microarray-based transcriptome-wide time series of mRNA expression, containing 16 independent measurements for both young and aged animals. Each individual time point consists of total RNA from hind limb skeletal muscles from 3 different animals.

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Circadian Dysfunction in Skeletal Muscle Impairs Limb Perfusion and Muscle Regeneration in Peripheral Artery Disease [Myotube-RNAseq]

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Circadian Dysfunction in Skeletal Muscle Impairs Limb Perfusion and Muscle Regeneration in Peripheral Artery Disease

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Circadian Dysfunction in Skeletal Muscle Impairs Limb Perfusion and Muscle Regeneration in Peripheral Artery Disease [Myotube-ATACseq]

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Circadian transcriptome of fast tibialis anterior (TA) and slow soleus (SOL) skeletal muscles from muscle-specific Bmal1 KO and control Cre- littermates

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2021-11-25 | PXD015616 | Pride

Deep proteome of aging skeletal muscles reveals Smoc2 as a modulator of satellite cell regenerative capacity

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Differentially expressed genes during disuse atrophy.

Project description:To identify atrophy genes directly targeted by Bcl-3 transactivator at a genome wide level, we performed whole transcript expression array and ChIP-seq for muscles from weight bearing or 5-day hind limb unloaded mice. Genes that showed increased expression with unloading and a Bcl-3 peak in the promoter (from ChIP-seq data) were considered as Bcl-3 direct targets during disuse atrophy. Using ChIP array, we identified 241 direct targets for Bcl-3. Our data describe Bcl-3 as a global regulator both of the proteolysis and the change in energy metabolism that are essential components of muscle atrophy due to disuse. Disuse skeletal muscle atrophy was induced by hind limb unloading. Weight bearing (WB) or 5-day hind limb unloaded (HU) muscles were harvested for total RNA isolation and processed for whole transcript expression profiling. We chose to examine gene expression and Bcl-3 binding from 5-day unloaded muscles because our previous time course study of disuse atrophy suggested that most genes are differentially regulated at this time point, and thus, would best represent the time for Bcl-3 binding to the gene targets of the NF-kB transcriptional network.

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RNA-Seq transcriptome profiling of soleus from adult and aged mice following disuse muscle atrophy and recovery

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2018-05-15 | GSE102284 | GEO

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