Mus musculus
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ABSTRACT:
PROVIDER: PRJNA96229 | ENA |
REPOSITORIES: ENA
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Project description:Common acute injuries to skeletal muscle can lead to significant pain and disability. The current therapeutic approaches for treating muscle injuries are dependent on the clinical severity but not on the type of injury. The aim of this study was to compare the molecular events accompanying the degeneration and repair phases of contraction- and trauma-induced muscle injuries by applying DNA microarray methodology to two well-characterized mouse models of skeletal muscle injury, i.e., eccentric contraction-induced injury (CI) and traumatic injury induced by freezing (FI). Histopathological evaluation and measurements of muscle strength were accompanied by analyses of expression for 12,488 known genes at four time points ranging from 6 hours to 7 days post-injury. Real-time RT-PCR was used to confirm some of the gene expression temporal profiles. While both types of injury cause early induction of transcription, myogenic, and stress-responsive factors, they also induce injury type-specific gene expression profiles. CI only activates a set of genes associated with the protection and repair of protein and structural integrity while FI activates gene sets which result in extensive inflammatory responses, tissue remodeling, angiogenesis, and myofibre and extracellular matrix synthesis. This study identified genes that are candidates for therapeutic manipulation following two disparate types of muscle injury. Experiment Overall Design: 2 types of skeletal muscle injury (eccentric contraction- and freeze-induced) x 4 time points after injury (6 hours, 1 day, 3 days, and 7 days post-injury). There were 3 samples for each of the 8 cells with the exception of the 'contraction injury, 1 day post-injury' and 'freeze injury, 7 days post-injury' cells; for each of these 2 cells, there were only 2 samples. Additionally, there were 3 control (i.e., uninjured) muscle samples.
2007-11-22 | E-GEOD-5413 | biostudies-arrayexpress
Project description:Influence of LKB1 on contraction-induced gene expression in skeletal muscle
| PRJNA293860 | ENA
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from Mus musculus tissues (Heart, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
2021-05-05 | PXD022309 | Pride
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from seven Mus musculus tissues (Heart, Brain, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
2018-04-24 | PXD007288 | Pride
Project description:HIF Prolyl Hydroxylase Inhibition Protects Skeletal Muscle from Contraction-Induced Injury
| PRJNA376517 | ENA
Project description:Common acute injuries to skeletal muscle can lead to significant pain and disability. The current therapeutic approaches for treating muscle injuries are dependent on the clinical severity but not on the type of injury. The aim of this study was to compare the molecular events accompanying the degeneration and repair phases of contraction- and trauma-induced muscle injuries by applying DNA microarray methodology to two well-characterized mouse models of skeletal muscle injury, i.e., eccentric contraction-induced injury (CI) and traumatic injury induced by freezing (FI). Histopathological evaluation and measurements of muscle strength were accompanied by analyses of expression for 12,488 known genes at four time points ranging from 6 hours to 7 days post-injury. Real-time RT-PCR was used to confirm some of the gene expression temporal profiles. While both types of injury cause early induction of transcription, myogenic, and stress-responsive factors, they also induce injury type-specific gene expression profiles. CI only activates a set of genes associated with the protection and repair of protein and structural integrity while FI activates gene sets which result in extensive inflammatory responses, tissue remodeling, angiogenesis, and myofibre and extracellular matrix synthesis. This study identified genes that are candidates for therapeutic manipulation following two disparate types of muscle injury. Keywords: time course, comparative genomic hybridization
2006-12-31 | GSE5413 | GEO
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from Mus musculus tissues (Heart, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
2024-11-07 | MSV000096332 | MassIVE
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from seven Mus musculus tissues (Heart, Brain, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
2024-11-07 | MSV000096331 | MassIVE
Project description:We analyzed the functional role of DOR (Diabetes and Obesity Regulated gene) (also named Tp53inp2) in skeletal muscle. We show that DOR has a direct impact on skeletal muscle mass in vivo. Thus, using different transgenic mouse models, we demonstrate that while muscle-specific DOR gain-of-function results in reduced muscle mass, loss-of-function causes muscle hypertrophy. DOR has been described as a protein with two different functions, i.e., a nuclear coactivator and an autophagy regulator (Baumgartner et. al., PLoS One, 2007; Francis et. al., Curr Biol, 2010; Mauvezin et. al., EMBO Rep, 2010; Nowak et. al., Mol Biol Cell, 2009). This is why we decided to analyze which of these two functions could explain the phenotype observed in our mice models. In this regard, we performed a transcriptomic analysis using microarrays looking for genes differentially expressed in the quadriceps muscle of WT and SKM-Tg mice as well as in C and SKM-KO animals. Surprisingly, only a reduced number of genes were dysregulated upon DOR manipulation and most of the genes underwent mild changes in expression. These data strongly suggest that DOR does not operate as a nuclear co-factor in mouse skeletal muscle under the conditions subjected to study. In contrast, DOR enhances basal autophagy in skeletal muscle and promotes muscle wasting when autophagy is a contributor to muscle loss. To determine the functional role of DOR in skeletal muscle, we generated transgenic mice (SKM-Tg) overexpressing DOR specifically in skeletal muscle under the Myosin-Light Chain 1 promoter/enhancer. The open reading frame of DOR was introduced in an EcoRI site in the MDAF2 vector, which contains a 1.5 kb fragment of the MLC1 promoter and 0.9 kb fragment of the MLC1/3 gene containing a 3' muscle enhancer element (Rosenthal et. al., PNAS, 1989; Otaegui et. al., FASEB J, 2003). The fragment obtained after the digestion of this construct with BssHII was the one used to generate both transgenic mouse lines. Nontransgenic littermates were used as controls for the transgenic animals (Wt). In addition, a muscle-specific DOR knock-out mouse line (SKM-KO) was also generated by crossing homozygous DOR loxP/loxP mice with a mouse strain expressing Cre recombinase under the control of the Myosin-Light Chain 1 promoter (Bothe et. al., Genesis, 2000). Deletion of exons 3 and 4 driven by Cre recombinase caused the ablation of DOR expression. Non-expressing Cre DOR loxP/loxP littermates were used as controls for knockout animals (C). Four-month-old male mice were used in all experiments. Mice were in a C57BL/6J pure genetic background.
2014-02-13 | GSE54917 | GEO
Project description:Comparison of murine masticatory and limb skeletal muscle
| PRJNA107007 | ENA