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The effects of MuRF1 knockout, sex, and a high fat diet consumption on gastrocnemius muscle transcriptomics.

ABSTRACT: The effects of MuRF1 knockout, sex, and a high fat diet consumption on gastrocnemius muscle transcriptomics.

PROVIDER: PRJNA742471 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14996504_1.fastq.gz	Fastqsanger.gz
	SRR14996504_2.fastq.gz	Fastqsanger.gz
	SRR14996505_1.fastq.gz	Fastqsanger.gz
	SRR14996505_2.fastq.gz	Fastqsanger.gz
	SRR14996506_1.fastq.gz	Fastqsanger.gz

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The effects of MuRF1 knockout, sex, and a high fat diet consumption on gastrocnemius muscle transcriptomics.

Project description:MuRF1 is an E3 ubiquitin ligase known to play a role in skeletal muscle atrophy. Our objectives in this study were to gain further insight into the roles MuRF1 plays in skeletal muscle and to determine if this is influenced by sex and/or consumption of a high fat diet. To address these objectives we used RNA sequencing to analyze the transcriptome of gastrocnemius muscle from 30 week old, MuRF1 knockout (-/-) and wild type, male and female mice fed a chow or high fat diet (HFD).

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MuRF1-dependent regulation of systemic carbohydrate metabolism as revealed from transgenic mouse studies

Project description:Under various pathophysiological muscle-wasting conditions like diabetes and starvation, a family of ubiquitin ligases, including MuRF1 (Muscle specific RING-Finger protein 1), are induced to target muscle proteins for degradation via ubiquitination. In an attempt to identify the in vivo targets of MuRF1 we have generated transgenic mouse lines overexpressing MuRF1 in a skeletal muscle specific fashion. MuRF1-TG lines were viable and had normal fertility. Characterization of their skeletal muscles did not reveal evidence for muscle wasting at 10 weeks of age. In this experiment we compared the skeletal muscle transcriptome of transgenic mice with wildtypes. Keywords: MuRF1 transgene overexpression

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Cardiac Muscle Ring Finger-1 (MuRF1) and Transcriptional Regulation of Ischemia-Reperfusion Injury In Vivo

Project description:We previously identified a role for the muscle-specific ubiquitin ligase MuRF1 (Muscle Ring Finger-1) in cardiac ischemia-reperfusion (I/R) injury. We found that cardiomyocyte-specific (alphaMHC-) MuRF1 transgenic mice (MuRF1 Tg+) mice were significantly protected from I/R injury. As we discovered MuRF1’s regulation of other transcriptions factors, we sought to identify other ways in which MuRF1 was cardioprotective in I/R injury. In the present study, we first identified the regulation of MuRF1 expression by qPCR in a porcine model of I/R injury. MuRF1 mRNA significantly increased within 90 minutes of I/R injury. We next assayed MuRF1 Tg+ ventricular tissue after I/R reperfusion injury by microarray (44K transcripts) to identify how MuRF1 regulates the transcriptome. We identified 71 significantly altered genes having a >1.5-fold (p<0.01) in MuRF1 Tg+ and wildtype hearts challenged with I/R injury (or sham operation). Functional annotation of the top upregulated genes found enrichment for myogenesis, cell adhesion, and nucleic acid metabolism. TRANSFAC analysis of MuRF1 Tg+ significant genes identified enrichment for genes (30-53%) with promoter regions recognized by the transcription factors MAZ, PIT1, VMW65, and BACH2. The transcription factor MAZ binds muscle creatine kinase (MCK) promoter in skeletal and cardiac myocytes, known most for its regulation of myogenin and MEF2C in cardiomyocytes. While the role of PIT1 and BACH2 in adult cardiomyocytes is not clear, VMW65 is a powerful transactivator with functions in chromatin remodeling. In neonatal cardiomycoyte I/R injury, VMW65 associates with HIF1alpha to upregulate cardioprotective VEGF, Glut-1, Glut-4, HSP70, and iNOS expression. These findings elucidate the MuRF1-specific regulation of genes in cardiac I/R injury that are associated with cardioprotection and may represent multiple additional direct or indirect mechanisms that MuRF1 regulates cardiomyocyte signaling.

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MuRF1 regulation of Fenofibrateâs induction of spontaneous cardiac hypertrophy in vivo.

Project description:MuRF1 -/- w/ Fenofibrate treatment leads to the reduction of proteolytic and fibrolytic enzymes, increasing hypertrophy Four strain-matched groups of 3-8 week old mice were investigated: 1) MuRF1 -/- Fenofibrate feed; 2) MuRF1 -/- chow feed; 3) MuRF1 +/+ Fenofibrate feed; 4) MuRF1 +/+ chow feed at two time points: 1) 3 weeks; 2) 8 Weeks Biological replicates: Two to three per condition. Hearts harvested. One replicate per array.

2016-03-01 | E-GEOD-68480 | biostudies-arrayexpress

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Sex Differences in the Skeletal Muscle Response to a High Fat, High Sucrose Diet in Rats

Project description:Men are diagnosed with type 2 diabetes at lower body mass indexes than women; the role of skel-etal muscle in this sex difference is poorly understood. Type 2 diabetes impacts skeletal muscle, particularly in females who demonstrate a lower oxidative capacity compared to males. To ad-dress mechanistic differences underlying this sex disparity, we investigated skeletal muscle mito-chondrial respiration in female and male rats in response to chronic high-fat, high-sugar (HFHS) diet consumption. Four-week-old Wistar Rats were fed a standard chow or HFHS diet for 14 weeks to identify sex-specific adaptations in mitochondrial respirometry and characteristics, transcrip-tional patterns, and protein profiles. Fat mass was greater with the HFHS diet in both sexes when controlled for body mass (p < 0.0001). Blood glucose and insulin resistance were greater in males (p = 0.01) and HFHS-fed rats (p < 0.001). HFHS-fed males had higher mitochondrial respiration compared with females (p < 0.01 sex/diet interaction). No evidence of a difference by sex or diet was found for mitochondrial synthesis, dynamics, or quality to support the mitochondrial respi-ration sex/diet interaction. However, transcriptomic analyses indicate sex differences in nutrient handling. Sex-specific differences occurred in PI3K/AKT signaling, PPARα/RXRα, and triacyl-glycerol degradation. These findings may provide insight into the clinical sex differences in body mass index threshold for diabetes development and tissue-specific progression of insulin re-sistance.

2024-03-31 | GSE228215 | GEO

Identification of the MuRF1 skeletal muscle ubiquitylome through quantitative proteomics

Project description:MuRF1 is a muscle-specific E3 ubiquitin ligase and component of the ubiquitin proteasome system. MuRF1 is transcriptionally upregulated under conditions that cause muscle loss, in both rodents and humans, and is a recognized marker of muscle atrophy. In this study, we used in vivo electroporation to determine if MuRF1 overexpression alone can cause muscle atrophy and, in combination with ubiquitin proteomics, identify the endogenous MuRF1 substrates in skeletal muscle. Tibialis anterior (TA) muscles were transfected with an untagged MuRF1 plasmid or control plasmid for 14 days. A total of 963 ubiquitination sites, corresponding to 250 proteins, were quantified from the TA muscle. Statistical analysis revealed that the overexpression of MuRF1 resulted in significant upregulation of 153 ubiquitination sites on 45 proteins and significant downregulation of 16 sites on 11 proteins. Substrates of MuRF1 include contractile and metabolic proteins, deubiquitinases, p62, and VCP. Moreover, MuRF1-mediated ubiquitination leads to destabilization and breakdown of the sarcomere and reveals a role for MuRF1 in the regulation of additional proteolytic pathways in skeletal muscle.

2021-07-07 | PXD023872 | Pride

MuRF1 regulation of Fenofibrate’s induction of spontaneous cardiac hypertrophy in vivo.

Project description:MuRF1 -/- w/ Fenofibrate treatment leads to the reduction of proteolytic and fibrolytic enzymes, increasing hypertrophy

2016-03-01 | GSE68480 | GEO

The histone H3 K4me3, K27me3 and K27ac genome-wide dis-tributions are differently influenced by sex in brain cortexes and gastrocnemius of the Alzheimer’s disease PSAPP mouse model

Project description:Background: Women represent the majority of Alzheimer’s disease patients and show typical symptoms. Genetic, hormonal and behavioral mechanisms have been proposed to explain gender differences in dementia prevalence. Whether sex differences exist in the epigenetic landscape of neuronal tissue during the progression of the disease is unknown. Methods: To investigate the differences of histone H3 modifications important for transcription we determined the ge-nome-wide profiles in K4me3, K27ac and K27me3 from brain cortexes of an Alzheimer mouse model (PSAPP). Gastrocnemius muscles were also tested since they are known to be different in the two sexes and are affected during the disease progression. Results: Correlation analysis dis-tinguished the samples based on sex for H3K4me3 and H3K27met3 but not for H3K27ac. The analysis of TSS signal distribution and of bounding sites revealed that the epigenetic landscape of gastrocnemius is more influenced than brain by sex, with the exception of H3K27me3 distribution on the X chromosome which showed sex-related differences in promoters belonging to behavior and cellular/ neuronal spheres in mice cortexes. Conclusions: The epigenetic landscape is slightly affected by sex in brain, with the exception of H3K27me3. On the other hand, a higher number of differences can be found in gastrocnemius.

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