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PW1/Peg3 expression regulates the key properties that determine mesoangioblast stem cell competence

ABSTRACT: Mesoangioblasts are vessel-associated progenitor cells that show therapeutic promise for the treatment of muscular dystrophy. Mesoangioblasts have the ability to undergo skeletal muscle differentiation and cross the blood vessel wall regardless of the developmental stage at which they are isolated. Here we show that PW1/Peg3 is expressed at high levels in mesoangioblasts obtained from mouse, dog and human tissues and its level of expression correlates with their myogenic competence. Silencing PW1/Peg3 markedly inhibits myogenic potential of mesoangioblasts in vitro through MyoD degradation. Moreover, lack of PW1/Peg3 abrogates mesoangioblast ability to cross the vessel wall and to engraft into damaged myofibers through the modulation of the junctional adhesion molecule-A. We conclude that PW1/Peg3 function is essential for conferring proper mesoangioblast competence and that the determination of PW1/Peg3 levels in human mesoangioblasts may serve as a biomarker to identify the best donor populations for therapeutic application in muscular dystrophies.

ORGANISM(S): Mus musculus

PROVIDER: GSE64334 | GEO | 2015/01/19

SECONDARY ACCESSION(S): PRJNA270758

REPOSITORIES: GEO

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PW1/Peg3 expression regulates the key properties that determine mesoangioblast stem cell competence

Project description:Mesoangioblasts are vessel-associated progenitor cells that show therapeutic promise for the treatment of muscular dystrophy. Mesoangioblasts have the ability to undergo skeletal muscle differentiation and cross the blood vessel wall regardless of the developmental stage at which they are isolated. Here we show that PW1/Peg3 is expressed at high levels in mesoangioblasts obtained from mouse, dog and human tissues and its level of expression correlates with their myogenic competence. Silencing PW1/Peg3 markedly inhibits myogenic potential of mesoangioblasts in vitro through MyoD degradation. Moreover, lack of PW1/Peg3 abrogates mesoangioblast ability to cross the vessel wall and to engraft into damaged myofibers through the modulation of the junctional adhesion molecule-A. We conclude that PW1/Peg3 function is essential for conferring proper mesoangioblast competence and that the determination of PW1/Peg3 levels in human mesoangioblasts may serve as a biomarker to identify the best donor populations for therapeutic application in muscular dystrophies. Ctrl Mesoangioblasts (MABs) transduced with a Lentiviral vector shControl (2 replicates, Ctrl_1 and Ctrl_2) and shPW1 Mesoangioblasts transduced with a Lentiviral vector shPW1 (2 replicates, PW1-siRna_1 and PW1-siRna_2)

2015-01-19 | E-GEOD-64334 | biostudies-arrayexpress

Gene profile of dystrophic cardiac progenitor cells

Project description:Cardiac resident stem/progenitor cells are intensively studied as a potential therapeutic tool for cardiomyopathies. While surface marker expression and ability to generate cardiomyocytes have been characterized in some detail for several types of these progenitors, little is known on how their cardiac differentiation is regulated. Beta sarcoglycan null (bSG KO) mice are a model for limb girdle muscular dystrophy type 2E (LGMD2E), and are characterized by muscular dystrophy and progressive dilated cardiomyopathy. In the present study we isolated and characterized cardiac progenitors (mesoangioblasts) from the small vessels of neonatal hearts bSG KO mice and unexpectedly observed that they differentiate spontaneously into skeletal muscle fibers both in vitro and when transplanted in regenerating muscles and infarcted hearts. The micro array data showed that dystrophic cardiac progenitor and myogenic cells (C2C12) share similar gene expression profile. Keywords: Beta sarcoglycan null mice, muscular dystrophy, cardiac mesoangioblasts, myogenic differentiation Biological triplicates of cardiac wild-type and dystrophic mesoangioblasts isolated from different heart region (atrium, ventricle, aorta) were compared. C2C12 cells were used as positive control for myogenic differentiation.

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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.

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

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Activation of imprinted gene Pw1 promotes cardiac fibrosis after ischemic injury [sham_and_MI]

Project description:The activation of fibroblasts and production of extracellular matrix (ECM) after cardiac injury has been the focus of research on cardiac fibrosis. Whether imprinted genes play a role in the fibrogenesis or extracellular matrix production after heart damage has not been studied. Here, we show that the imprinted gene Pw1 directed ECM production by regulating de novo purine synthesis (DNPB) after myocardial infarction (MI). After MI, the DNA methylation of the imprinting control region (ICR) of Pw1 gene in the injured area was reduced and both alleles of Pw1 in fibroblasts are activated. Further, loss of Pw1 in fibroblasts can enhance cardiac function, reduce cardiac fibrosis and extracellular matrix secretion after cardiac injury. To screen the targets of PW1, we contrasted chromatin immunoprecipitation (ChIP)-seq and RNA-seq using the injured left ventricles at 7 days post-MI, we next found PW1 binds directly upstream of the Pfas gene that encodes one of the DNPB enzymes phosphoribosylformylglycinamidine synthase (PFAS) in heart after injury. Similarly, specific knockout of pfas in fibroblasts also improves cardiac function and reduces ECM production. Moreover, de novo purine biosynthesis is necessary for ECM production in activated fibroblasts. These observations implicate understanding the mechanism of Pw1 in the repair of cardiac injury will provide new ideas for the treatment of cardiovascular diseases.

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