Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Angiogenesis and Gene Signature in Muscular Hypertrophy

ABSTRACT: Adult myogenic progenitor cells (activated satellite cells) express both HGF and its receptor cMet. Following muscle injury, autocrine HGF-Met stimulation plays a key role in promoting activation and early division of satellite cells. Magic-F1 (Met-Activating Genetically Improved Chimeric Factor-1) is an HGF-derived, engineered protein that contains two Met-binding domains that promotes muscle hypertrophy, protecting myogenic precursors against apoptosis, increasing their fusion ability and enhancing muscle differentiation. Hemizygous and homozygous Magic-F1 transgenic mice displayed constitutive muscle hypertrophy. We described here microarray analysis on Magic-F1 myogenic progenitor cells showing an altered gene signatures involving muscle hypertrophy and vasculogenesis compared to wild-type cells. In parallel, we performed a functional analysis on homozygous Magic-F1 transgenic mice versus control, demonstrating that Magic-F1+/+ mice display impairment on running performance. Finally, we show that induced muscle hypertrophy affects positively vascular network, increasing vessel number in fast twitch fibers. This is due to unique features of mammalian skeletal muscle and its remarkable ability to adapt promptly to different physiological demands by changing gene expression profile. Biological triplicates of Magic-F1+/+ and control satellite cells were used for microarray analysis.

ORGANISM(S): Mus musculus

SUBMITTER: Flavio Ronzoni

PROVIDER: E-GEOD-83771 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Transcriptome analysis of satellite cells isolated from an animal model of skeletal muscle hypertrophy

Project description:Skeletal muscle is a post-mitotic tissue with unique plasticity. It has an extraordinary ability to adjust to changes in its physiological environment by altering its metabolic phenotype and its mass. Satellite cells are the most important myogenic progenitor cells involved in muscle regeneration and remodeling. The activation of these cells is governed by genetic programs involving complex transcriptional responses and can be involved in muscle hypertrophy adaptations. We described here gene expression variations evaluated by microarray analysis in satellite cells isolated from wild type and Magic-F1 transgenic mice, a model of skeletal muscle hypertrophy. The transcriptome analysis shows an altered gene signature in proliferating Magic-F1 satellite cells compared to controls, involving genes associated to muscle growth and vasculogenesis.

2016-06-28 | GSE83771 | GEO

Comparing gene expression between PICs and satellite cells from 1 week old muscle

Project description:The satellite cell is considered the major tissue-resident stem cell underlying muscle regeneration, however, multiple non-satellite cell myogenic progenitors have been identified. PW1/Peg3 is expressed in satellite cells as well as a subset of interstitial cells with myogenic potential termed PICs (PW1+ Interstitial Cells). PICs differ from satellite cells by their anatomical location (satellite cells are sublaminal and PICs are interstitial), they do not express any myogenic marker and arise from a Pax3-independent lineage. Upon isolation from juvenile muscle (1 to 3 weeks old), PICs are capable to form both skeletal and smooth muscle suggesting they constitute a more plastic population compared to satellite cells. We used microarrays to gain insight into the relantionship between PICs and satellite cells. PICs and satellite cells were isolated from 1-week old mouse muscle and subsequent RNA extraction was performed.

2012-09-01 | E-GEOD-40523 | biostudies-arrayexpress

Notch signaling/MyoD double deficient embryonic muscle progenitors

Project description:Skeletal muscle growth and regeneration rely on myogenic progenitor and satellite cells, the stem cells of postnatal muscle. Elimination of Notch signals during mouse development results in premature differentiation of myogenic progenitors and formation of very small muscle groups. Here we show that this drastic effect is rescued by mutation of the muscle differentiation factor MyoD. However, rescued myogenic progenitors do not assume a satellite cell position and contribute poorly to myofiber growth. The disrupted homing is due to a deficit in basal lamina assembly around emerging satellite cells and to their impaired adhesion to myofibers. On a molecular level, emerging satellite deregulate the expression of basal lamina components and adhesion molecules like integrin a7, collagen XVIIIa1, Megf10 and Mcam. We conclude that Notch signals control homing of satellite cells, stimulating them to contribute to their own microenvironment and to adhere to myofibers. Gene expression analysis using total RNA from FACS-isolated Vcam-1+/CD31-/CD45-/Sca1- embryonic muscle progenitor cells from E17.5 back muscle tissue of MyoD-/-, Pax3cre/+;Rbpjflox/flox;MyoD-/- and Pax3cre/+;DnMamlflox/flox;MyoD-/- mice.

2012-12-31 | E-GEOD-39379 | biostudies-arrayexpress

Comparing gene expression between PICs and satellite cells from 1 week old muscle

2012-09-01 | GSE40523 | GEO

Notch signaling/MyoD double deficient embryonic muscle progenitors

2012-12-31 | GSE39379 | GEO

Transcription profiling of mouse muscle satellite cell-derived myoblasts (MyoD-/-, p53-/-)

Project description:Muscle satellite cells are a self-renewing pool of stem cells that give rise to daughter myogenic precursor cells in adult skeletal muscle. Published and preliminary data indicated that MyoD and p53 genes are involved in satellite cell differentiation. We would like to know what downstream genes of both transcription factors are affected in satellite cell-derived myoblasts (MyoD-/-, p53 -/-). Experiment Overall Design: this experiment include 3 samples and 25 replicates

2008-06-12 | E-GEOD-3244 | biostudies-arrayexpress

The NAD+-Dependent SIRT1 Deacetylase Translates a Metabolic Switch into Regulatory Epigenetics in Skeletal Muscle Stem Cells

Project description:Selective genetic ablation of the SIRT1 deacetylase domain in skeletal muscle results in increased H4K16 acetylation and deregulated activation of the myogenic program in satellite cells To establish the role of the deacetylase SIRT1 in skeletal muscle we examined the genome wide distribution of H4K16ac in quiescent (FI) and proliferating (Cul) satellite cells isolated from WT mice (C57Bl/6 background) and SIRT1mKO (generated via breeding of Pax7cre/+ knock-in mice with mice containing the floxed exon 4 SIRT1 allele). We also analyzed the distribution of SIRT1 in quiescent and proliferating FACS isolated WT satellite cells (two replicates). We generated the mRNA profiles (at least two replicate for each experiment) of FACS isolated quiescent, proliferating and differentiating (1 day in differentiation medium) satellite cells of WT mice and SIRT1mKO. The selective genetic ablation of the SIRT1 deacetylase domain in skeletal muscle results in increased H4K16 acetylation and deregulated activation of the myogenic program.

2015-01-30 | E-GEOD-64379 | biostudies-arrayexpress

Expression data from murine myogenic cells

Project description:Skeletal muscle has great regenerative capacity, which is dependent on muscle stem cells, also known as satellite cells. We established the purification system of myogenic cells. We used microarrays to identify specific genes during the muscle regenerative process. Myogenic cells were purified at regenerative stages for RNA extraction and hybridization on Affymetrix microarrays. CTX-2d and CTX-5d are the samples derived from injured muscles 2 days and 5 days after cardiotoxin-injection, respectively.

2014-07-01 | E-GEOD-56903 | biostudies-arrayexpress

Expression data of satellite cells through muscle injury time course

Project description:Satellite cells are resident skeletal muscle stem cells responsible for muscle maintenance and repair. In resting muscle, satellite cells are maintained in a quiescent state. Satellite cell activation induces the myogenic commitment factor, MyoD, and cell cycle entry to facilitate transition to a population of proliferating myoblasts that eventually exit the cycle and regenerate muscle tissue. The molecular mechanism involved in the transition of a quiescent satellite cell to a transit-amplifying myoblast is poorly understood. We used microarrays to detail the global program of gene expression of in vivo satellite cell activation through muscle injury and identified RNA post-transcriptional regulation as a key component of satellite cell activation. Wild type or Sdc4-/- satellite cells were FACS isolated from resting muscle or from muscle 12h and 48h following barium chloride-induced muscle injury. 5000 cell equivalents of RNA was labeled and hybridized to MOE430v2 GeneChips (Affymetrix) and scanned as per manufacturers protocol. Probeset intensities were GCRMA normalized for further analysis including UPGMA hierarchical clustering, analysis of variance (ANOVA), and fold change.

2012-07-31 | E-GEOD-38870 | biostudies-arrayexpress

Discrete subsets of myogenic and mesenchymal precursors give rise to soft tissue sarcomas of distinct lineage differentiation

Project description:This work examines sarcoma formation within discrete subsets of KRAS(G12V)-expressing p16p19null myogenic and mesenchymal cells found normally in skeletal muscle. We show that prospectively isolated skeletal muscle precursor cells (SMPs) within the satellite cell pool can serve as cancer cells-of-origin for mouse rhabdomyosarcomas (soft tissue sarcomas with features of myogenic differentiation). Alternatively, non-myogenic progenitors (ScaPCs) induce sarcomas lacking myogenic differentiation markers.

2011-11-10 | GSE22841 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data