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Hochuekkito accelerates recovery from cisplatin induced-muscle atrophy accompanied by slow-twitch fiber-specific microRNA upregulation in mice

ABSTRACT: Hochuekkito accelerates recovery from cisplatin induced-muscle atrophy accompanied by slow-twitch fiber-specific microRNA upregulation in mice

PROVIDER: PRJNA1255521 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33313739.fastq.gz	Fastqsanger.gz
	SRR33313740.fastq.gz	Fastqsanger.gz
	SRR33313741.fastq.gz	Fastqsanger.gz
	SRR33313742.fastq.gz	Fastqsanger.gz
	SRR33313743.fastq.gz	Fastqsanger.gz

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Hochuekkito accelerates recovery from cisplatin induced-muscle atrophy accompanied by slow-twitch fiber-specific microRNA upregulation in mice

Project description:Hochuekkito (HET) increased locomotor activity and muscle weight in cisplatin induced muscle atrophy model mice, probably by enhancing myogenesis in slow-twitch fibers, which was related to miRNA expression changes. Thus, HET may be useful in treating cisplatin-induced muscle atrophy.

2025-05-15 | GSE295648 | GEO

Increased global DNA methylation by Dnmt3a disrupts skeletal muscle homeostasis, promotes age-related muscle atrophy, and reduces muscle metabolic elasticity

Project description:Loss of muscle mass and function—a hallmark of skeletal muscle aging—is known as sarcopenia. Moreover, mammalian aging is reportedly driven by loss of epigenetic information. However, the effect of epigenetic alterations on skeletal muscle homeostasis is unknown. In this study, we show that chronic elevation of global DNA methylation results in a myopathy-like phenotype and age-related changes in skeletal muscle. Overexpression of muscle de novo methyltransferase 3a (Dnmt3a) increased central nucleus-positive myofibers, predominantly in fast-twitch myofibers, and shifted muscle fiber type to stress-resistant slow-twitch myofibers, accompanied by increased inflammatory and senescent signatures, decreased mitochondrial OXPHOS complex I protein level, and reduced basal autophagy in skeletal muscle. Chronic Dnmt3a overexpression decreased muscle mass and strength, and impaired tolerance to endurance exercise with age. This age-related decline in endurance exercise capacity was accompanied by an augmented inflammatory signature in a manner that is enhanced with age and promoted muscle atrophy. Network analysis identified Akt1 as a potential hub gene. Dnmt3a expression not only reduced sensitivity to starvation-induced muscle atrophy by suppressing the FoxO-regulated autophagy and ubiquitin–proteasome systems, but also reduced the restorability from starvation-induced muscle atrophy. These data suggest that increased global DNA methylation disrupts skeletal muscle homeostasis, promotes age-related muscle atrophy, and reduces muscle metabolic elasticity.

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Musashi 2 regulates normal hematopoiesis and accelerates leukemogenesis

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Molecular insights into human soleus muscle atrophy development: long-term dry immersion effects on the transcriptomic profile and post-translational signaling

Project description:Muscle disuse results in complex signaling alterations followed by structural and functional changes, such as atrophy, force decrease and slow-to-fast fiber-type shift. Little is known about human skeletal muscle signaling alterations under long-term muscle disuse. In this study, we describe the effects of 21-day dry immersion on human postural soleus muscle. We performed both transcriptomic analysis and Western blots to describe the states of the key signaling pathways regulating soleus muscle fiber size, fiber-type, and metabolism. 21-day dry immersion resulted in both slow-type and fast-type myofibers atrophy, downregulation of rRNA content, and mTOR signaling. 21-day dry immersion also leads to slow-to-fast fiber-type and gene expression shift, upregulation of p-eEF2, p-CaMKII, p-ACC content and downregulation of NFATc1 nuclear content. It also caused massive gene expression alterations associated with calcium signaling, cytoskeletal parameters, and downregulated mitochondrial signaling (including fusion, fission, and marker of mitochondrial density).

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Project description:Myofiber size regulation is critical in health, disease, and aging. MuSK (muscle-specific kinase) is a BMP (bone morphogenetic protein) co-receptor that promotes and shapes BMP signaling that is expressed at all neuromuscular junctions and is also present extrasynaptically in the slow soleus muscle. To investigate the role of the MuSK-BMP pathway in vivo we generated mice lacking the BMP-binding MuSK Ig3 domain. These ∆Ig3-MuSK mice are viable and fertile with innervation levels comparable to wild type. In 3-month-old mice myofibers are smaller in the slow soleus, but not in the fast TA. Here we use bulk RNA-seq to perform transcriptomic analysis of slow and fast mouse muscle. RNAseq analysis revealed soleus-selective decreases in RNA metabolism and protein synthesis pathways as well as dysregulation of IGF1 pathway components. Moreover, Akt-mTOR signaling is reduced in soleus but not TA. We propose that the MuSK-BMP pathway acts extrasynaptically to maintain myofiber size in slow muscle by promoting protein synthetic pathways including the IGF1-Akt-mTOR signaling. These results reveal a novel mechanism for regulating myofiber size in slow muscle and introduce the MuSK-BMP pathway as a target for promoting muscle growth and combatting atrophy.

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Transcription profiling by array of denervated muscular atrophy

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Differences in gene expression between fast and slow muscle or between normal and denervated slow muscles

2014-10-04 | GSE62028 | GEO

Differences in gene expression between fast and slow muscle or between normal and denervated slow muscles

Project description:Fast and slow skeletal muscles show different characteristics and phenotypes. This data obtained from microarray includes the comparison of normal fast plantaris and slow soleus muscles of adult rats. Characters of slow muscle are strongly dependent on the level of muscular activity. Denervation silences the muscular activity. Therefore, we determined the effects of denervation on gene expression in slow soleus muscle of adult rats. Denervation was performed by transection (~5 mm) of left sciatic nerve at the gluteal level. No treatments were made in the normal control rats. Sampling of soleus and/or plantaris was performed in both normal and experimental groups 28 days after the surgery.

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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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