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Gastrocnemius muscle-Deletion of TECRL promotes skeletal muscle repair

ABSTRACT: Gastrocnemius muscle-Deletion of TECRL promotes skeletal muscle repair

PROVIDER: PRJNA1067623 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27682263_1.fastq.gz	Fastqsanger.gz
	SRR27682263_2.fastq.gz	Fastqsanger.gz
	SRR27682264_1.fastq.gz	Fastqsanger.gz
	SRR27682264_2.fastq.gz	Fastqsanger.gz

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Gastrocnemius muscle-Deletion of TECRL promotes skeletal muscle repair

Project description:Myogenic regeneration relies on the proliferation and differentiation of satellite cells. TECRL (Trans-2,3-Enoyl-CoA Reductase Like) is an endoplasmic reticulum protein only expressed in cardiac and skeletal muscle. However, its role in myogenesis remains unknown. We show that TECRL expression is increased in response to ischemic injury. Satellite cell-specific deletion of TECRL enhances muscle repair by increasing the expression of EGR2 through the activation of the ERK1/2 signaling pathway, which in turn promotes the expression of PAX7. We further showed that TECRL deletion led to the upregulation of the histone acetyltransferase general control non-derepressible 5 (GCN5), which enhances the transcription of EGR2 through acetylation.

2024-05-29 | GSE253890 | GEO

Analysis of gastrocnemius muscle from chow-fed control and skeletal muscle specific Cpt1b knockout mice

Project description:To determine the transcriptomic effects of Cpt1b loss on skeletal muscle gene expression, we assessed gastrocnemius muscle in chow-fed control and Cpt1b skeletal muscle specific knockout mice using a serial analysis of gene expression strategy. Complementary bioinformatics pathway enrichment studies were performed which indicated that differentially expressed genes between genotypes were predominantly related to various processes include carbohydrate metabolism, lipid metabolism, amino acid metabolism, cell proliferation, and apoptosis.

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Differentially modulated transcriptomes of mouse skeletal muscle (gastrocnemius) during postnatal development

Project description:Purpose: During postnatal development the fetal skeletal muscle undergoes a rapid and dramatic transition to adult function through transcriptional and post-transcriptional mechanisms, including alternative splicing (AS) Methods:We performed RNA-seq for high-resolution analysis of transcriptome changes during postnatal mouse skeletal muscle development using RNA from gastrocnemius muscle from embryonic day 18.5, postnatal day 2 (PN2), PN14, PN28, adult (22 weeks). Results: We identified a novel role for AS in several cellular functions including calcium handling and membrane organization during postnatal skeletal muscle development. Furthermore, AS transitions within calcium handling genes are responsive to Celf1 and Mbnl1, RNA-binding proteins with developmentally regulated expression. Conclusions: We identified a novel role for AS in several functional categories during postnatal development including calcium handling, vesicular trafficking and cell junctions.

2017-12-22 | GSE108402 | GEO

Transcription profiling ofmouse skeletal muscle to investigate the effect profiling ofacute muscle unloading on soleus and gastrocnemius muscle gene expression

Project description:Gene expression changes induced by acute skeletal muscle unloading, which leads to physiological changes including muscle atrophy, fibre-type switching, and loss of ability to transition between lipid and glucose as energy source (metabolic inflexibility), was investigated by hind-limb suspension (HLS) treatment of Male ICR mice (28â32 g body wt; Harlan, Indianapolis, IN). Agilent Whole Mouse Genome Oligo Microarrays were utilised to examine the effects of HLS on mRNA expression profiles of the soleus muscle and the gastrocnemius muscle in the hindlimbs of freely ambulating control and 24h HLS treated mice. Experiment Overall Design: Five independent biological replicates of this experiment (Control and HLS) were carried out.

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Direct contribution of skeletal muscle mesenchymal progenitors to bone repair

Project description:Bone regeneration involves skeletal stem/progenitor cells within periosteum and bone marrow, the formation of a fibrous callus followed by the deposition of cartilage and bone matrix to consolidate the fracture. Interactions between bone and skeletal muscle are known to play a role in bone repair but the underlying mechanisms are poorly understood. To better understand the role of skeletal muscle during bone repair, we characterized stem/progenitor cells within skeletal muscle that participate in bone repair. We show that cells originating from bone marrow, periosteum and skeletal muscle are all derived from the Prx1 embryonic lineage. We developed a mouse polytrauma model combining a non-stabilized tibial fracture and mechanical injury to adjacent skeletal muscles. In this polytrauma model, bone fracture healing is impaired. We characterized the Prx1-derived cell population within skeletal muscle in response to fracture and to polytrauma. To do so, we performed fracture and polytrauma in Prx1Cre;Rosa mTmG mice. We harvested skeletal muscle surrounding the tibia at d0 (uninjured), and surrounding the fracture site at d3 and d5 post-fracture or post-polytrauma. Following enzymatic and mechanical digestion of skeletal muscle tissue, we FACS sorted Prx1-derived GFP+ cells and sequenced them using the 10X Chromium technology.

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Project description:The processes by which mitochondria respond to cellular energy demands brought on by physiologic and pathophysiologic stimuli are essential to cellular adaptation and organismal survival. Disrupted mitochondrial function is implicated in several human disease states, underscoring the need to elucidate the molecular mechanisms that control mitochondrial function and metabolism. We previously described a patient with a gain-of-function mutation in Site-1 Protease (S1P) who exhibited idiopathic hyperCKemia, myoedema, and altered muscle mitochondrial morphology. To date, S1P has been heavily characterized in liver and bone, with very little known about its potential function in skeletal muscle. In our current study, we generated a skeletal muscle-specific S1P knockout mouse line (S1PsmKO) to examine the role of S1P in skeletal muscle. S1PsmKO mice were overtly normal in their appearance and health. However, examination of 12-week-old S1PsmKO mice showed increased gastrocnemius muscle mass and aged S1PsmKO mice exhibited increased muscle mass in both gastrocnemius and soleus relative to age-matched controls. Moreover, isolated muscle from S1PsmKO exhibited increased maximal mitochondrial respiration relative to floxed littermates (controls). RNA-Seq analysis showed increased transcript numbers of the mitochondrial-resident gene, Mss51 in S1PsmKO gastrocnemius relative to control mice. Mss51 is a member of the TGF-β/MSTN pathway, which controls mitochondrial metabolism. Similar to S1PsmKO muscle, S1P-depleted C2C12 cells also had increased maximal respiration, which was reversed by exogenous MSS51 expression. These data identify S1P as a regulator of muscle mass and mitochondrial metabolism, and implicate S1P as a novel modulator of TGF-β signaling. Method: Male mice were maintained on standard chow diet until 12 weeks of age.

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Loss of skeletal muscle Bmal1 +/- Acute Exercise

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Differentially modulated transcriptomes of mouse skeletal muscle (gastrocnemius) during postnatal development

Project description:Differentially modulated transcriptomes of mouse skeletal muscle (gastrocnemius) during postnatal development

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