The effect of BMP4/6 stimulation on adult muscle stem cells (MuSC)
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PROVIDER: PRJNA525422 | ENA |
REPOSITORIES: ENA
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Project description:The effect of BMP4 and BMP6 stimulation on adult muscle stem cells (MuSC)
| PRJNA669835 | ENA
Project description:Muscle development and regeneration strongly depends on extracellular cues and growth factors, which are taken up by muscle stem cells and guide them either towards proliferation and fusion or towards quiescence. Here we investigated the effect of bone morphogenetic protein (BMP) signaling on Pax7 positive adult muscle stem cells of the mouse. We discovered a cross talk between the BMP- and NOTCH-signalling pathways, leading to high upregulation upon BMP4/BMP6-stimulation of Hes1 mRNA which is a key component of the NOTCH-siganling pathway.
2023-10-01 | GSE127798 | GEO
Project description:Muscle development and regeneration strongly depends on extracellular cues and growth factors, which are taken up by muscle stem cells and guide them either towards proliferation and fusion or towards quiescence. Here we investigated the effect of bone morphogenetic protein (BMP) signaling on Pax7 positive adult muscle stem cells of the mouse. We discovered a cross talk between the BMP- and NOTCH-signalling pathways, leading to high upregulation upon BMP4/BMP6-stimulation of Hes1 mRNA which is a key component of the NOTCH-siganling pathway.
2023-10-01 | GSE159594 | GEO
Project description:We previously showed that STAT3 regulates myoblast differentiation in cell culture models, yet its role in adult muscle satellite cells (MuSC) in vivo was less well characterized. When Stat3 was conditionally deleted in MuSC, muscle development and adult MuSC formation were not affected. However, with repeated muscle injuries, the number of the quiescent MuSC in STAT3-null mice decreased and the regeneration was delayed, suggesting defective MuSC maintenance. Consistently, when we conditionally deleted Stat3 in MuSC of dystrophin-null mice, a mouse model for the fatal human Duchenne muscular dystrophy, the adult double knockout (dKO) mice displayed age-dependent reduction in the number of MuSC, and increase in muscle inflammation and fibrosis. Mechanistically, Stat3 ablation in dystrophin-null MuSC resulted in downregulation of several key myogenic genes including Pax7, upregulation of multiple pro-inflammatory and pro-fibrotic genes, and an increase in fibroadipogenic progenitor cells, which collectively contributed to defective MuSC maintenance and aggravated inflammation and fibrosis in dKO mice.
2016-07-13 | GSE68736 | GEO
Project description:The capacity of muscle to grow or to regenerate is provided by adult stem cells, called satellite cells. Satellite cells can generate proliferating myoblasts, sensitive to MP signaling. To understand the role of this signaling pathway in adult myogenesis, we analyzed the changes in gene expression following treatment of primary myoblasts with BMP4 agonist or GREM1 antogonist. Here we used microarrays and to clarify BMP4/GREM1 signaling and we identified several pathways and cellular processes affected.
2021-01-01 | GSE145694 | GEO
Project description:Skeletal muscle stem cells (MuSC), also called satellite cells, are indispensable for maintenance and regeneration of adult skeletal muscles. Yet, a comprehensive picture of the regulatory events controlling the fate of MuSC is missing. Here, we determine the proteome of MuSC to design a loss-of-function screen, and identify 120 genes important for MuSC function including the arginine methyltransferase Prmt5. MuSC-specific inactivation of Prmt5 in adult mice prevents expansion of MuSC, abolishes long-term MuSC maintenance and abrogates skeletal muscle regeneration. Interestingly, Prmt5 is dispensable for proliferation and differentiation of Pax7(+) myogenic progenitor cells during mouse embryonic development, indicating significant differences between embryonic and adult myogenesis. Mechanistic studies reveal that Prmt5 controls proliferation of adult MuSC by direct epigenetic silencing of the cell cycle inhibitor p21. We reason that Prmt5 generates a poised state that keeps MuSC in a standby mode, thus allowing rapid MuSC amplification under disease conditions.
2015-03-13 | GSE66822 | GEO
Project description:Impaired skeletal muscle stem cell (MuSC) function has long been suspected to contribute to the pathogenesis of muscular dystrophy (MD). Here we describe that defects in the endothelial cell (EC) compartment of the perivascular stem cell niche in three different types of MD are associated with inefficient mobilization of MuSCs following tissue damage. Using chemoinformatic analysis, we identified the 13 amino acid form of the peptidic hormone apelin (AP-13) as a candidate for systemic stimulation of skeletal muscle ECs. In dystrophic mice, administration of AP-13 generates a pro-myogenic EC-rich niche that supports MuSC function and markedly improves tissue regeneration, muscle strength, and physical performance. Moreover, we demonstrate that EC specific knockout of the AP-13 receptor leads to regenerative defects that phenocopy major pathological features of MD. Altogether, we provide in vivo proof-of-concept that enhancing endogenous repair by targeting the perivascular niche is a viable therapeutic avenue for MD and characterize AP-13 as a novel drug candidate for systemic treatment of stem cell dysfunction.
2024-03-20 | GSE240983 | GEO
Project description:Adult muscle stem cells (MuSC) are quiescent with a localization between myofibers and basal lamina. Upon injury, MuSC exit quiescence, reenter cell cycle, expand and differentiate for muscle regeneration. By using genetic mouse model, we identified p110α/mTORC1 signaling as a indispensable pathway that permits quiescence exit and cell cycle reentry. In order to dig out the downstream effectors, we compared the transcriptome of freshly isolated MuSC from Ctrl (p110α-f/+:R26-YFP/YFP:Pax7-CreER/CreER) to MuSC-specific p110α-null (iKO, p110α-f/f:R26-YFP/YFP:Pax7-CreER/CreER) mice by RNA-sequencing, and AP1 target genes were dramatically down-regulated in iKO MuSC. Restoration of Jun could significantly rescue the cell cycle reentry defect in iKO MuSC. In summary, we provided a p110α/mTORC1/Jun axis required for quiecence exit and cell cycle reentry of MuSC.
2018-02-25 | GSE109472 | GEO
Project description:Muscle stem cells (MuSC) exhibit distinct behaviors during successive phases of developmental myogenesis. However, how their transition to adulthood is regulated is poorly understood. Here we show that fetal MuSC resist progenitor specification and exhibit altered division dynamics, intrinsic features that are progressively lost postnatally. Following transplantation, fetal MuSC more efficiently expand and contribute to muscle repair. Conversely, the efficiency of niche colonization increases in adulthood, indicating a balance between muscle growth and stem cell pool repopulation. Gene expression profiling identified several extracellular matrix (ECM) molecules preferentially expressed in fetal MuSC, including tenascin-C, fibronectin and collagen VI. Loss-of-function experiments confirmed their essential and stage-specific role in regulating MuSC function. Finally, fetal-derived paracrine factors were able to enhance adult MuSC regenerative potential. Together, these findings demonstrate that MuSC change the way in which they remodel their microenvironment to direct stem cell behavior in support of the unique demands of muscle development or repair. MuSCs were isolated through fluorescent-activate cell sorting usinf alpha7-integirn and CD34 as markers to identify the cell population. Total mRNA was then isolated, and samples at different developmental times were compared.
2016-01-20 | E-GEOD-76989 | biostudies-arrayexpress
Project description:This experiment was carried out to identify the short-term effects of Activin A and BMP4 stimulation on gene expression in human embryonic stem cells grown in a chemically defined medium. Keywords: Growth factor stimulation experiment
2008-03-12 | GSE9060 | GEO