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Study of the signaling modulated by HDAC4 in skeletal muscle in ALS

ABSTRACT: Study of the signaling modulated by HDAC4 in skeletal muscle in ALS

PROVIDER: PRJNA498450 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8110284.fastq.gz	Fastqsanger.gz
	SRR8110285.fastq.gz	Fastqsanger.gz
	SRR8110286.fastq.gz	Fastqsanger.gz
	SRR8110287.fastq.gz	Fastqsanger.gz

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Study of the signaling modulated by HDAC4 in skeletal muscle in ALS

Project description:BACKGROUND: Histone deacetylase 4 (HDAC4) has been proposed as a target for the treatment of Amyotrophic Lateral Sclerosis (ALS) because it mediates nerve-skeletal muscle interaction and since its expression in skeletal muscle correlates with the severity of the disease. However, our recent studies on the skeletal muscle response upon long-term denervation highlighted the importance of HDAC4 in maintaining muscle integrity. METHODS: To fully identify the yet uncharacterized HDAC4 functions in ALS, we genetically deleted HDAC4 in skeletal muscles of a mouse model of ALS. Body weight, skeletal muscle, innervation and spinal cord were analyzed over time by morphological and molecular analyses. A transcriptome analysis was also performed to delineate the signaling modulated by HDAC4 in skeletal muscle of a mouse model of ALS. FINDINGS: HDAC4 deletion in skeletal muscle caused earlier ALS onset, characterized by body weight loss, muscle denervation and atrophy, and compromised muscle performance in ALS mice, although the main catabolic pathways were not activated. A transcriptome analysis identified the gene networks modulated by HDAC4 in ALS, revealing UCP1 as a top regulator that may be implicated in worsening ALS features. INTERPRETATION: HDAC4 plays an important role in preserving innervations and skeletal muscle in ALS, likely by modulating the UCP1 gene network. Our study highlights a possible risk in considering HDAC inhibitors for the treatment of ALS.

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The growth factor FGF21 maintains neuromuscular junction through histone deacetylase HDAC4 in denervation-induced skeletal muscle atrophy

Project description:Skeletal muscles undergo atrophy in response to denervation and neuromuscular diseases. Understanding the mechanisms by which denervation drives muscle atrophy is crucial for developing therapies against neurogenic muscle atrophy. Here, we identify muscle-secreted fibroblast growth factor 21 (FGF21) as a key inducer of atrophy following muscle denervation. In denervated skeletal muscles, Fgf21 is the most robustly upregulated member of the Fgf family and acts in an autocrine/paracrine manner to promote muscle atrophy. Silencing Fgf21 in muscle prevents denervation-induced muscle wasting by preserving neuromuscular junction (NMJ) innervation. Conversely, forced expression of FGF21 in muscle reduces NMJ innervation, leading to muscle atrophy. Mechanistically, TGFB1 released by denervated fibro-adipogenic progenitors (FAPs) upregulates Fgf21 through the JNK/c-Jun axis. The resulting increase in FGF21 protein reduces the cytoplasmic level of histone deacetylase 4 (HDAC4), culminating in muscle atrophy. HDAC4 knockdown abolishes the atrophy-resistant effects observed in Fgf21-deficient denervated muscles, resulting in muscle atrophy. Our findings reveal a novel role and heretofore unrecognized mechanism of FGF21 in skeletal muscle atrophy, suggesting that inhibiting muscular FGF21 could be a promising strategy for mitigating skeletal muscle atrophy.

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Samples from mouse skeletal muscle

Project description:samples from mouse Skeletal Muscle, analysis different expression profiling<br>HDAC4：Sciatic nerve transection model was prepared after injection of HDAC4-shRNA lentivirus into the tibialis anterior muscle of mice. 14 days later, tibialis anterior muscle was obtained. DenSciatic nerve transection model was prepared after injection of empty vector virus into the tibialis anterior muscle of mice. 14 days later, tibialis anterior muscle was obtained. N: The empty vector virus was injected into muscles from the sham group. 14 days later, tibialis anterior muscle was obtained.

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Transcription profiling of skeletal muscle from amyotrophic lateral sclerosis sod1(G86R) axotomized mice and control mice to monitor denervation-dependent gene expression in an Amyotrophic lateral sclerosis (ALS) mouse model

Project description:Amyotrophic lateral sclerosis (ALS) is a fatal adult-onset neuromuscular disorder characterized by the selective degeneration of upper and lower motor neurons, progressive muscle wasting and paralysis. To define the full set of alterations in gene expression in skeletal muscle during the course of the disease, we performed high-density oligonucleotide microarray analysis of gene expression in hind limb skeletal muscles of sod1(G86R) mice, one of the existing transgenic models of ALS. To monitor denervation-dependent gene expression, we determined the effects of short-term acute denervation on the muscle transcriptome after sciatic nerve axotomy.

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