Endogenous Muscle Atrophy F-box is Involved in the Development of Cardiac Rupture After Myocardial Infarction
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE97494 | GEO | 2017/04/07
SECONDARY ACCESSION(S): PRJNA381988
REPOSITORIES: GEO
Similar Datasets
Project description:Muscle atrophy F-box (MAFbx) is an E3 ubiquitin ligase which plays a critical role in mediating skeletal muscle atrophy. We investigated the effect of MAFbx KO in cardiac hypertrophy in response to pressure overload. A DNA microarray analysis was conducted using total RNA prepared from wild type and MAFbx KO mouse hearts subject to transverse aortic constriction (TAC). Results provide insight into the molecular mechanism to mediate the effect of MAFbx upon pathological hypertrophy.
2011-05-01 | GSE24372 | GEO
Project description:Muscle atrophy F-box (MAFbx) is an E3 ubiquitin ligase which plays a critical role in mediating skeletal muscle atrophy. We investigated the effect of MAFbx KO in cardiac hypertrophy in response to pressure overload. A DNA microarray analysis was conducted using total RNA prepared from wild type and MAFbx KO mouse hearts subject to transverse aortic constriction (TAC). Results provide insight into the molecular mechanism to mediate the effect of MAFbx upon pathological hypertrophy. We applied TAC to wild type and MAFbx KO mice, and extracted total RNA one week after the surgery. The gene expression profiles were examined by Affymetrix Mouse Gene ST Array.
2011-05-01 | E-GEOD-24372 | biostudies-arrayexpress
Project description:Cardiomyocyte cell death and renewal are the pivotal events in the pathogenesis of heart failure .Atrogin-1/MAFbx is an ubiquitin E3 ligase that regulates myocardial structure and function through the cellular mechanism of protein degradation. We used DNA microarrays to detail the global trends in gene expression underlying atrogin-1- overexpressed cardiomyocytes and identified distinct classes of up-regulated genes during this process. Our findings suggest that atrogin-1 plays a critical role in regulating cardiac dysfunction at transcriptional level and may provide novel insight into how atrogin-1 modulates the programming of cardiac muscle gene expression.
2011-08-03 | GSE31117 | GEO
Project description:Cardiomyocyte cell death and renewal are the pivotal events in the pathogenesis of heart failure .Atrogin-1/MAFbx is an ubiquitin E3 ligase that regulates myocardial structure and function through the cellular mechanism of protein degradation. We used DNA microarrays to detail the global trends in gene expression underlying atrogin-1- overexpressed cardiomyocytes and identified distinct classes of up-regulated genes during this process. Our findings suggest that atrogin-1 plays a critical role in regulating cardiac dysfunction at transcriptional level and may provide novel insight into how atrogin-1 modulates the programming of cardiac muscle gene expression. Cardiomyocytes were infected with GFP control or atrogin-1 adenoviruses for RNA extraction and hybridization on Affymetrix microarrays. We sought to define the effects of atrogin-1 on the global programme of gene expression in primary cardiomyocytes. To that end, neonatal rat cardiomyocytes were infected with GFP control (G) or atrogin-1 adenovirus (A) for 24 hours.
2011-08-02 | E-GEOD-31117 | biostudies-arrayexpress
Project description:Belt electrode-skeletal muscle electrical stimulation (B-SES) involves the use of belt-shaped electrodes to simultaneously contract multiple muscle groups. Twitch contractions have been demonstrated to protect against denervation-induced muscle atrophy in rats, possibly via mitochondrial biosynthesis. In this study, we examined whether inducing tetanus contractions with B-SES suppresses muscle atrophy and identified the underlying molecular mechanisms. We evaluated the effects of acute (60 Hz, 5 min) and chronic (60 Hz, 5 min, every alternate day for 1 week) B-SES on the tibialis anterior (TA) and gastrocnemius (GAS) muscles in Sprague Dawley rats using belt electrodes attached to both ankle joints. In acute stimulation, a significant decrease in glycogen content in the left and right TA and GAS was observed, suggesting that B-SES causes simultaneous contractions in multiple muscle groups. B-SES also enhanced p70S6K phosphorylation, an indicator of the mechanistic target of rapamycin complex 1 activity. During chronic stimulations, rats were divided into control (CONT), denervation-induced atrophy (DEN), and DEN+electrically stimulated with B-SES (DEN＋ES) groups. After 7 days of treatment, muscle wet weight (n = 8-11 for each group) and muscle fiber cross-sectional area (CSA, n = 6 for each group) of the TA and GAS muscles were reduced in the DEN and DEN+ES groups compared to those in the CON group. The DEN+ES group showed significantly higher muscle weight and CSA than the DEN group. Although RNA-seq and pathway analysis suggested that mitochondrial and ribosome biogenesis are key events in this phenomenon, mitochondrial content showed no difference. In contrast, ribosomal RNA 28S and 45S (n = 6) levels in the DEN+ES group were higher than those in the DEN group. The mRNA levels of the muscle proteolytic molecules Atrogin-1 and MuRF1 were significantly higher in DEN than in CONT but were suppressed in DEN+ES. In conclusion, tetanic electrical stimulation of both ankles using belt electrodes was effective in preventing denervation-induced atrophy in multiple muscle groups. Unlike twitch contractions, ribosomal biosynthesis plays a key role in tetanic contractions to prevent muscle atrophy.
2024-01-06 | E-MTAB-13286 | biostudies-arrayexpress
Project description:Disuse atrophy is a common clinical phenomenon which significantly impacts muscle function and activities of daily living. In this study, we did expression profiling to identify transcriptional pathways associated with muscle remodeling in a clinical model of disuse. Keywords: Differentiation design
2007-08-28 | GSE8872 | GEO
Project description:Disuse atrophy is a common clinical phenomenon which significantly impacts muscle function and activities of daily living. In this study, we did expression profiling to identify transcriptional pathways associated with muscle remodeling in a clinical model of disuse. Keywords: Differentiation design 28 Skeletal muscle biopsies from the medial gastrocnemius in patients with an ankle fracture (4 patients, 8 profiles) and from healthy volunteers (2 subjects, 4 profiles) subjected to 4-11 days of mobilization, as well as from the non-immobilized contralateral legs (16 profiles).
2007-08-28 | E-GEOD-8872 | biostudies-arrayexpress
Project description:Skeletal muscle atrophy is a debilitating condition associated with weakness, fatigue, and reduced functional capacity. Nuclear factor-kappaB (NF-κB) transcription factors play a critical role in atrophy. Knockout of genes encoding p50 or the NF-κB co-transactivator, Bcl-3, abolish disuse atrophy and thus they are NF-κB factors required for disuse atrophy. We do not know however, the genes targeted by NF-κB that produce the atrophied phenotype. Here we identify the genes required to produce disuse atrophy using gene expression profiling in wild type compared to Nfkb1 (gene encodes p50) and Bcl-3 deficient mice. There were 185 and 240 genes upregulated in wild type mice due to unloading, that were not upregulated in Nfkb1-/- and Bcl-3-/- mice, respectively, and so these genes were considered direct or indirect targets of p50 and Bcl-3. All of the p50 gene targets were contained in the Bcl-3 gene target list. Most genes were involved with protein degradation, signaling, translation, transcription, and transport. To identify direct targets of p50 and Bcl-3 we performed chromatin immunoprecipitation of selected genes previously shown to have roles in atrophy. Trim63 (MuRF1), Fbxo32 (MAFbx), Ubc, Ctsl, Runx1, Tnfrsf12a (Tweak receptor), and Cxcl10 (IP-10) showed increased Bcl-3 binding to κB sites in unloaded muscle and thus were direct targets of Bcl-3. p50 binding to the same sites on these genes either did not change or increased, supporting the idea of p50:Bcl-3 binding complexes. p65 binding to κB sites showed decreased or no binding to these genes with unloading. Fbxo9, Psma6, Psmc4, Psmg4, Foxo3, Ankrd1 (CARP), and Eif4ebp1 did not show changes in p65, p50, or Bcl-3 binding to κB sites, and so were considered indirect targets of p50 and Bcl-3. This work represents the first study to use a global approach to identify genes required to produce the atrophied phenotype with disuse. 24 mice were used based on 4 mice per group, 3 mouse genotypes (wild type, Nfkb1-/-, Bcl3-/-) and 2 conditions (weight-bearing and unloaded).
2011-01-10 | E-GEOD-23497 | biostudies-arrayexpress
Project description:Musculoskeletal diseases such as muscular dystrophy, cachexia, osteoarthritis, and rheumatoid arthritis impair overall physical health. Patients suffer from increased pain and death rate, decreased productivity and function. Inflammation and fibrosis are commonly observed in musculoskeletal disorders either at the bone, muscle, or joint. The Interleukin-6 Family of Cytokines primarily Interleukin-6 (IL-6) are implicated in the context of musculoskeletal disorders. In this study, we utilized adeno-associated virus expressing murine Oncostatin M or an empty vector at 10^11 viral particles to observe effects in muscle and bone of mice in the presence and absence of Interleukin-6. We performed echocardiography, microCT, quantitative polymerase chain reaction, histology, and RNA-sequencing to characterize the functional effects on muscle and bone. The echocardiography results demonstrated cardiac dysfunction as shown by reduced ejection fraction (%) and fractional shortening (%) with AAV-Osm compared to AAV-Null. RNA-sequencing results on cardiac muscle showed increased cardiac inflammation and fibrosis genes with AAV-Osm. Skeletal muscle weights and histology revealed muscle atrophy and fibrosis in the gastrocnemius, tibialis anterior, and quadriceps of the local limbs injected with AAV-Osm, but not observed in the non-injected side. MicroCT results revealed local and distant trabecular bone loss with AAV-Osm as shown by reduced bone volume, number, thickness, and increased trabeculae separation. Our findings show that Oncostatin M induces cardiac dysfunction, muscle, and bone atrophy independent of Interleukin-6.
2022-10-04 | GSE185996 | GEO
Project description:To assess changes in the muscle proteome that due to tumor burden and dexamethasone treatments and compare proteomic changes that occur in atrophy due to tumor burden and dexamethasone treatment with atrophy caused by aging. Regulators of muscle atrophy induced by diseases such as cancer or drugs such as dexamethasone are largely unknown. We would therefore like to determine the proteomic signature of atrophying muscle caused by tumor burden (LLC cell injected mice) and dexamethasone treatment in order to examine possible biomarkers and regulators of muscle atrophy. We would also like to compared the proteomic signature of different modes of muscle atrophy to determine similarities and differences in the possible biomarkers and regulators.
2022-02-22 | PXD027490 | Pride