ABSTRACT: To survey altered gene expression in MG56-knockout muscle, total RNA preparations from mouse hindlimb muscle and hearts were subjected to gene microarray analysis. Results exhibit the effects of MG56 deficiency on overall transcription, and may further imply the biological role of MG56. Total RNA samples were preparated from Tibialis-anterior (TA) muscle and hearts of three P9 MG56-knockout mice and the corresponding wild-type mice were mixed and then subjected to Affymetrix Mus musculus microarrays.
Project description:To survey altered gene expression in MG56-knockout muscle, total RNA preparations from mouse hindlimb muscle and hearts were subjected to gene microarray analysis. Results exhibit the effects of MG56 deficiency on overall transcription, and may further imply the biological role of MG56.
Project description:p53 regulates a distinct subset of skeletal muscle mRNAs during immobilization-induced skeletal muscle atrophy For additional details see Fox et al, p53 and ATF4 mediate distinct and additive pathways to skeletal muscle atrophy during limb immobilization. Am J Physiol Endocrinol Metab. 2014 Aug 1;307(3):E245-61. Bilateral tibialis anterior muscles were harvested at three days for the following conditions: 1) hindlimb immobilization of C57BL/6 mice; 2) hindlimb immobilization of p53 mKO and littermate control mice; 3) transfection of wild type mice with p53 plasmid or control plasmid
Project description:Transcript data from tibialis anterior muscle from male muscle-specific Coactivator-Associated Arginine Methyltransferase 1 (Carm1 ) knockout mice (Carm1 skm-/- ) and wild-type mice (Carm1 skm+/+) generated by using the Cre-loxP system (on a C57BL6J/129 background) with HSA-Cre mice (from Jackson laboratories). We used RNA-Seq to detail the effects of muscle-specific loss of Carm1 on the global program of gene expression in tibialis anterior muscle.
Project description:This study examines the transcriptional profile at a single-nuclei resolution in mice with muscle-specific deletion of the aryl hydrocarbon receptor (AHR). Wildtype (AHRfl/fl, floxed Cre negative littermates) and AHRmKO (AHR muscle specific knockout) mice were given chronic kidney disease via adenine supplemented diet. Mice were then subjected to femoral artery ligation as an experimental model of peripheral artery disease. Tibialis anterior muscles were harvested at five days post-surgery and immediately snap frozen in liquid nitrogen and stored at -80C until nuclei isolation. In both libraries, muscle specimens were pooled from three males prior to nuclei isolations were performed.
Project description:Mice were electrically stimulated by implanting a pacer. The hindlimb muscles received low frequency stimulation for three hours and the tibialis anterior muscle was harvested at different time points after the stimulation. Sham operated control mice were included in the experiment. mRNA was pooled from 6 mice at each time point and hybridized to the arrays together with mRNA from untreated mice (reference). Keywords: time-course
Project description:Skeletal muscle is a highly adaptive tissue that changes with many physiological stimuli and is composed of many cell types. Upon muscle injury, the concerted action of these cells is required to proceed through the process of inflammation, extracellular matrix remodeling, and restoration of function. To uncover novel genes and molecular pathways important for skeletal muscle remodeling and regeneration, we used a mouse hindlimb unloading and reloading protocol, and performed transcriptomics analysis. This study focuses on the microprotein Mustn1 (Musculoskeletal embryonic nuclear protein 1, also known as Mustang), whose gene expression is increased in muscle at the onset of hindlimb reloading, exercise, and injury. We generated a whole-body Mustn1 knockout mouse model and performed proteomics analysis of muscle and aorta.
Project description:We identified genes expressed in mouse skeletal muscle, during the process of muscle regeneration after injury, which are dysregulated in the absence of Mef2a expression. MEF2A is a member of the evolutionarily conserved MEF2 transcription factor family which has known roles in cardiac muscle development and function, but is not well studied in skeletal muscle. We performed a comparison of gene expression profiles in wild type and MEF2A knockout tibialis anterior muscle, seven days post-injury with cardiotoxin. The results indicated that a variety of genes expressed during muscle regeneration, predominantly microRNAs in the Gtl2-Dio3 locus, are dysregulated by the loss of MEF2A expression. Skeletal muscle RNA used in the present study included the following two sample groups: (WT) pooled total RNA from tibialis anterior muscle taken from 5 wild type mice at seven days post-injury with 10uM cardiotoxin; (KO) pooled total RNA from tibialis anterior muscle taken from 5 Mef2a knockout mice at seven days post-injury with 10uM cardiotoxin. All mice were between 2-4 months of age. Both male and female mice were used.
Project description:C57Bl6 mice were subjected to cecal-ligation and puncture or sham surgery. Mice were sacrificed after 24 h or 96 h and muscle tissue was harvested. RNA from tibialis anterior muscle was isolated and subjected to RNA sequencing.
Project description:To investigate the molecular mechanisms governing the transition of skeletal muscle from atrophy to compensatory regeneration and hypertrophy, we employed a mouse model involving hindlimb unloading and subsequent reloading, conducting a comprehensive analysis of global gene expression using RNA-sequencing (RNA-seq). Gastrocnemius muscle samples were obtained from three groups: control mice, mice subjected to 10 days of hindlimb unloading-induced muscle atrophy, and mice reintroduced to normal cage activity for 1 day following the unloading period (reloading).
Project description:Total RNA was isolated from 3 WT and 3 ERRalpha null hearts and independent hybridizations were performed using MOE430 2.0 microarrays. Expression profiling was conducted to determine changes in gene expression in hearts lacking ERRa. The expression of genes involved in heart and muscle development, muscle contraction, lipid metabolism, OxPhos, protein metabolism and transcription were affected by the loss of ERRa. Experiment Overall Design: 3 hearts from WT and 3 hearts from ERRalpha-null mice were used in the study. The expression of genes in the ERRalpha KO hearts were compared to the reference WT hearts.