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Age-related gene expression signature in limb skeletal muscles and the diaphragm in mice and rats [mouse]

ABSTRACT: As a result of aging, skeletal muscle undergoes atrophy and a decrease in function. This age-related skeletal muscle weakness is known as “sarcopenia.” To understand the changes in gene expression that occur as a result of age in skeletal muscles, we generated a multi-time point gene expression signature throughout the lifespan of mice and rats, as these are the most commonly used species in preclinical research and intervention testing

ORGANISM(S): Mus musculus

PROVIDER: GSE226117 | GEO | 2023/06/19

REPOSITORIES: GEO

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Project description:As a result of aging, skeletal muscle undergoes atrophy and a decrease in function. This age-related skeletal muscle weakness is known as “sarcopenia.” To understand the changes in gene expression that occur as a result of age in skeletal muscles, we generated a multi-time point gene expression signature throughout the lifespan of mice and rats, as these are the most commonly used species in preclinical research and intervention testing

2023-06-19 | GSE226118 | GEO

Effect of muscle-specific ATF4 gene knockout (ATF4 mKO) on skeletal muscle mRNA levels in aged mice.

Project description:For additional details see Ebert et al, Identification and Small Molecule Inhibition of an ATF4-dependent Pathway to Age-related Skeletal Muscle Weakness and Atrophy.

2015-09-03 | GSE72658 | GEO

Effects of ursolic acid and tomatidine on skeletal muscle mRNA expression in aged mice.

Project description:For additional details see Ebert et al, Identification and Small Molecule Inhibition of an ATF4-dependent Pathway to Age-related Skeletal Muscle Weakness and Atrophy.

2015-09-03 | GSE72651 | GEO

Regulation of muscle mass by Thrombospondin-1

Project description:Loss of muscle mass is a pathological driver in both chronic illness and aging. We have discovered that skeletal muscle specific thrombospondin-1 (Thbs1) transgenic mice have profound muscle atrophy with age-dependent decreases in exercise capacity and premature lethality. Here, we compared the transcriptional profiles of skeletal muscle from control non-transgenic mice with those overexpressing Thbs1 in order to elucidate the transcriptional changes underlying the observed effects on skeletal muscle mass. The overall purpose was to identify new, effective targets to combat muscle atrophy and sarcopenia.

2024-04-18 | GSE245663 | GEO

LncRNA data in gastrocnemius muscles from mice that have undergone denervation of the right sciatic nerve or not

Project description:This study was to identify lncRNAs responsible for muscle atrophy Muscle atrophy commonly occurs in aging, disuse, starvation, and many chronic diseases including heart failure and cancer. Muscle atrophy leads to muscular weakness and reduced quality of life, which also significantly increases morbidity and mortality. While progress has been made in understanding the molecular underpinnings of muscle atrophy, currently there are no effective approved drugs to combat muscle atrophy. Thus, novel therapies for muscle atrophy would address an important unmet clinical need. Long non-coding RNAs (LncRNAs) are transcribed RNAs longer than 200 nucleotides with little or no protein-coding capacity. Several lncRNAs have been reported in myogenesis and few lncRNAs have been mechanistically linked to skeletal muscle diseases. Here we want to identify a lncRNA as a common regulator of multitypes of muscle atrophy.

2021-01-06 | GSE151300 | GEO

Cyclo His-Pro halts skeletal muscle degeneration and cardiomyopathy in murine myopathy models

Project description:Among the inherited myopathies, a group of muscular disorders characterized by structural and metabolic impairments in skeletal muscle, Duchenne muscular dystrophy (DMD) stands out for its devastating progression. Caused by the absence of functional dystrophin, DMD pathogenesis is driven by the progressive degeneration of muscle fibers, resulting in the development of inflammation and fibrosis that ultimately affect the overall muscle biomechanics. On the opposite end of the spectrum of muscle diseases, age-related sarcopenia is a common disease that affects a growing proportion of the elderly, often leading to frailty and loss of independence. Although characterized by fundamentally different pathological mechanisms, DMD and sarcopenia share the development of progressive muscle weakness and tissue inflammation. The natural compound Cyclo Histidine-Proline (CHP) has been shown to reduce inflammation and fibrosis in a number of metabolic diseases, including steatohepatitis and diabetes. We evaluate here the effects of CHP in DMD and sarcopenia. In two independent studies in the mdx mouse model of DMD, we show that CHP restored muscle contractility and force production, accompanied by a robust reduction of fibrosis and inflammation in skeletal muscle. In the mdx model, CHP furthermore prevented the development of cardiomyopathy and fibrosis in the diaphragm, the two leading causes of death for DMD patients. CHP also attenuated muscle atrophy and functional deterioration in a mouse model of age-related sarcopenia. These data in two different models of muscle dysfunction hence warrant further study of the effects of CHP in muscle pathologies in animal models and eventually in patients.

2024-05-11 | GSE241771 | GEO

Effect of muscle-specific ATF4 gene knockout (ATF4 mKO) on skeletal muscle mRNA levels in aged mice.

Project description:For additional details see Ebert et al, Identification and Small Molecule Inhibition of an ATF4-dependent Pathway to Age-related Skeletal Muscle Weakness and Atrophy. Quadriceps femoris muscles were harvested from 22-month-old muscle-specfic ATF4 knockout (ATF4 mKO) mice and littermate controls. mRNA levels in ATF4 mKO muscles were normalized to levels in littermate control muscles.

2015-09-03 | E-GEOD-72658 | biostudies-arrayexpress

MiRNA expression profiling of skeletal muscles in aged rodents

Project description:Skeletal muscle atrophy is one of the critical issues which elderly people face. The precise mechanism underlying muscle atrophy during aging is not fully understood. In order to identify miRNA whose expression is changed in age-associated muscle atrophy, we performed miRNA expression profiling of skeletal muscles in young and aged rats. Microarray analysis revealed differential miRNA expression in EDL and soleus muscles of aged rats compared with those of young rats. We next investigated whether the age-associated changes of miRNA expression observed in rats were recapitulated in mice and found that the expression level of miR-206 in EDL muscle and that of miR-196a in EDL and soleus muscles were respectively higher and lower in aged rodents than in young rodents. In mouse C2C12 myoblasts and myotubes, introduction of miR-196a decreased the protein level of Forkhead-box transcription factor Foxo1, a known target of miR-196a, indicating that miR-196a may regulate Foxo1 expression also in skeletal muscles. Furthermore, miR-196a overexpression exacerbated cell death caused by an exposure to hydrogen peroxide. Lastly, we demonstrated that expression of Foxo1 was elevated in EDL and soleus muscles of aged mice compared with those of young mice. These results suggest that miRNAs are involved in skeletal muscle atrophy during aging and that decreased miR-196a expression may protect skeletal muscle cells from oxidative stress in part through induction of Foxo1.

2016-08-31 | GSE70990 | GEO

Novel Sarcopenia-related Alterations in Sarcomeric Protein Post-translational Modifications in Skeletal Muscles Identified by Top-down Proteomics

Project description:Sarcopenia, the age-related loss of skeletal muscle mass and strength, is a significant cause of morbidity in the elderly and is a major burden on health care systems. Unfortunately, the underlying molecular mechanisms in sarcopenia remain poorly understood. Herein, we utilized top-down proteomics to elucidate sarcopenia-related changes in the fast- and slow-twitch skeletal muscles of aging rats with a focus on the sarcomeric proteome, which includes both myofilament and Z-disc proteins--the proteins that constitute the contractile apparatuses.

2017-06-12 | MSV000081157 | MassIVE

Resistance Exercise Reverses Aging in Human Skeletal Muscle

Project description:Human aging is associated with skeletal muscle atrophy and functional impairment (sarcopenia). Multiple lines of evidence suggest that mitochondrial dysfunction is a major contributor to sarcopenia. We evaluated whether healthy aging was associated with a transcriptional profile reflecting mitochondrial impairment and whether resistance exercise could reverse this signature to that approximating a younger physiological age. Skeletal muscle biopsies from healthy older (N = 25) and younger (N = 26) adult men and women were compared using gene expression profiling, and a subset of these were related to measurements of muscle strength. 14 of the older adults had muscle samples taken before and after a six-month resistance exercise-training program. Before exercise training, older adults were 59% weaker than younger, but after six months of training in older adults, strength improved significantly (P<0.001) such that they were only 38% lower than young adults. As a consequence of age, we found 596 genes differentially expressed using a false discovery rate cut-off of 5%. Prior to the exercise training, the transcriptome profile showed a dramatic enrichment of genes associated with mitochondrial function with age. However, following exercise training the transcriptional signature of aging was markedly reversed back to that of younger levels for most genes that were affected by both age and exercise. We conclude that healthy older adults show evidence of mitochondrial impairment and muscle weakness, but that this can be partially reversed at the phenotypic level, and substantially reversed at the transcriptome level, following six months of resistance exercise training. Keywords: resistance exercise, muscle, aging

2007-07-16 | GSE8479 | GEO

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