Human pluripotent stem cell-derived myogenic progenitor cells engraft to become quiescent functional satellite cells in vivo
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ABSTRACT:
PROVIDER: PRJNA693189 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13482463.fastq.gz | Fastqsanger.gz | |||
| SRR13482464.fastq.gz | Fastqsanger.gz |
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Project description:In this study, we generated human pluripotent stem cell-derived myogenic progenitor cells and transplanted into injured skeletal muscle. We performed two single cell RNA-seq experiments. In the first experiment, we compared transplanted satellite cells with in vitro controls. In the second study, we did a time-series analysis of transplanted cells.
2021-01-20 | GSE165075 | GEO
Project description:The acquisition of a proliferating cell status from a quiescent state as well as the shift between proliferation and differentiation are key developmental steps in skeletal-muscle stem cells (satellite cells) to provide proper muscle regeneration. However, how satellite-cell proliferation is regulated, though, is not fully understood. Here, we report that the c-isoform of the transcription factor Pitx2 increases cell proliferation in myoblasts by down-regulating the miRNAs miR-15b, miR-23b, miR-106b, and miR-503. This Pitx2c-miRNA pathway also regulates cell proliferation in early-activated satellite cells, enhancing the Myf5+ satellite cells and thereby promoting their commitment to a myogenic cell fate. This study reveals unknown functions of several miRNAs in myoblast and satellite-cell behaviour and thus may have future applications in regenerative medicine. mirVana microarrays (Ambion) were used to profile microRNA signature at different Pitx2 overexpression conditions, namely two different doses (4 and 8 µg CMV-Pitx2c plasmid, respectively) after 24 hours of transfection in SOL8 skeletal myogenic cells. 20 µg of total RNA was used to hybridize two distinct microRNA microarrays on each condition analyzed.
2015-06-10 | E-GEOD-53943 | biostudies-arrayexpress
Project description:The satellite cell of skeletal muscle provides a paradigm for quiescent and activated tissue stem cell states. We have carried out transcriptome analyses by comparing satellite cells from adult skeletal muscles, where they are mainly quiescent, with cells from growing muscles, regenerating (mdx) muscles, or with cells in culture, where they are activated. Our study gives new insights into the satellite cell biology during activation and in respect with its niche. We used microarrays to study the global programme of gene expression underlying adult satellite cell quiescence compared to activation states and to identify distinct classes of up-regulated genes in these two different states Skeletal muscle satellite cells were isolated by flow cytrometry using the GFP fluorescence marker from Pax3GFP/+ mice skeletal muscle. The transcriptome of quiescent satellite cells from adult Pax3GFP/+ muscle was compared to the transcriptome of activated satellite cells obtained from three different samples: 1) regenerating Pax3GFP/+:mdx/mdx muscle (Ad.mdx) , 2) growing 1 week old Pax3GFP/+ muscle (1wk), and 3) adult Pax3GFP/+ cells after 3 days in culture (Ad.cult).
2010-01-04 | E-GEOD-15155 | biostudies-arrayexpress
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
Project description:The influence of the extracellular matrix (ECM) within the stem cell niche remains poorly understood. We found that Syndecan-4 (Sdc4) and Frizzled-7 (Fzd7) form a coreceptor complex in satellite cells and that binding of the ECM glycoprotein Fibronectin (FN) to Sdc4 stimulates the ability of Wnt7a to induce the symmetric expansion of satellite stem cells. Newly activated satellite cells dynamically remodel their niche via transient high-level expression of FN. Knockdown of FN in prospectively isolated satellite cells severely impaired their ability to repopulate the satellite cell niche. Conversely, in vivo overexpression of FN with Wnt7a dramatically stimulated the expansion of satellite stem cells in regenerating muscle. Therefore, activating satellite cells remodel their niche through autologous expression of FN that provides feedback to stimulate Wnt7a signaling through the Fzd7/Sdc4 coreceptor complex. Thus, FN and Wnt7a together regulate the homeostatic levels of satellite stem cells and satellite myogenic cells during regenerative myogenesis. The data set contains one microarray of pooled quiescent skeletal muscle satellite cells
2014-07-11 | E-GEOD-59272 | biostudies-arrayexpress
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.
2012-08-01 | GSE38870 | GEO
Project description:The contribution of non-resident, non-satellite myogenic progenitors to postnatal muscle homeostasis and repair is controversial. Precursor cells with the capacity to generate striated muscle fibers in vitro have been isolated from diverse adult tissues, although their physiological role being currently unclear. Since murine dermis-derived precursor cell cultures generate striated muscle when transplanted in vivo, we pursued to identify and characterize the myogenic cell population present in dermis-derived sphere cultures. Lineage tracing experiments for myogenic, perivascular and dermal precursor cell lineages showed a major contribution of Myf5 and Pax7-positive cell progeny to the dermal myogenic precursor cell subset. Tracing, in situ localization and ultrastructural analyses unequivocally demonstrated that Panniculus carnosus muscle-derived satellite stem cells expand in the dermal sphere culture conditions and originate dermis-derived myofibers in vitro. These results highlight the importance of unraveling distinct lineages in sphere cultures to avoid wrong assumptions when determining the developmental potential of adult stem cells. strain: Crl:CD1(ICR), B6.129S4-Myf5tm3(cre)Sor /J, B6,FVB-Tg(Cspg4-cre)1Akik/J, B195AP-Cre
2017-02-21 | GSE67693 | GEO
Project description:The acquisition of a proliferating cell status from a quiescent state as well as the shift between proliferation and differentiation are key developmental steps in skeletal-muscle stem cells (satellite cells) to provide proper muscle regeneration. However, how satellite-cell proliferation is regulated, though, is not fully understood. Here, we report that the c-isoform of the transcription factor Pitx2 increases cell proliferation in myoblasts by down-regulating the miRNAs miR-15b, miR-23b, miR-106b, and miR-503. This Pitx2c-miRNA pathway also regulates cell proliferation in early-activated satellite cells, enhancing the Myf5+ satellite cells and thereby promoting their commitment to a myogenic cell fate. This study reveals unknown functions of several miRNAs in myoblast and satellite-cell behaviour and thus may have future applications in regenerative medicine.
2015-06-10 | GSE53943 | GEO
Project description:We performed genome-wide gene expression analysis of quiescent/activated muscle stem cells isolated from mouse skeletal muscle by flow cytometry. We analyzed the global changes in gene expression occurring within muscle stem cells (satellite cells) in homeostatic conditions or after cardiotoxin (CTX) injury (3 days). Pure satellite cell populations from dissociated skeletal muscle from mice were isolated using a well-established flow cytometry protocol gating on integrin a7(+) (positive selection) and Lin- (CD31, CD45, CD11b, Sca1) (negative selection).
2015-06-30 | E-GEOD-70376 | biostudies-arrayexpress
Project description:DNA methylation is an essential form of epigenetic regulation responsible for cellular identity. In muscle stem cells, termed satellite cells, DNA methylation patterns are tightly regulated during differentiation. However, it is unclear how these DNA methylation patterns affect the function of satellite cells. We demonstrate that a key epigenetic regulator, ubiquitin like with PHD and RING finger domains 1 (Uhrf1), is activated in proliferating myogenic cells but not expressed in quiescent satellite cells or differentiated myogenic cells in mice. Ablation of Uhrf1 in mouse satellite cells impairs their proliferation and differentiation, leading to failed muscle regeneration. Uhrf1-deficient myogenic cells exhibited aberrant up-regulation of transcripts, including Sox9, with the reduction of DNA methylation level of their promoter and enhancer region. These findings show that Uhrf1 is a critical epigenetic regulator of proliferation and differentiation in satellite cells, by controlling cell type-specific gene expression via maintenance of DNA methylation.
2022-02-04 | GSE169193 | GEO