RNA-seq for miRNAs in fibrocyte-adipocyte progenitors (FAPs) or myogenic progenitors (MPs) during muscle regeneration
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB16345 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR1698680.fastq.gz | Fastqsanger.gz | |||
| ERR1698681.fastq.gz | Fastqsanger.gz | |||
| ERR1698682.fastq.gz | Fastqsanger.gz | |||
| ERR1698679.fastq.gz | Fastqsanger.gz |
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Project description:Fibrosis is a deleterious invasion of tissues associated with many pathological conditions, such as Duchenne muscular dystrophy (DMD) for which no cure is at present available for its prevention or its treatment. Fibro-adipogenic progenitors (FAPs) are resident cells in the human skeletal muscle and can differentiate into myofibroblasts, which represent the key cell population responsible for fibrosis. In this study, we delineated the pool of microRNAs (miRNAs) that are specifically modulated by TGFβ1 in FAPs versus myogenic progenitors (MPs) by a global miRNome analysis. A subset of candidates, including several "FibromiRs", was found differentially expressed between FAPs and MPs and was also deregulated in DMD versus healthy biopsies. Among them, the expression of the TGFβ1-induced miR-199a~214 cluster was strongly correlated with the fibrotic score in DMD biopsies. Loss-of-function experiments in FAPs indicated that a miR-214-3p inhibitor efficiently blocked expression of fibrogenic markers in both basal conditions and following TGFβ1 stimulation. We found that FGFR1 is a functional target of miR-214-3p, preventing the signaling of the anti-fibrotic FGF2 pathway during FAP fibrogenesis. Overall, our work demonstrates that the « FibromiR » miR-214-3p is a key activator of FAP fibrogenesis by modulating the FGF2/FGFR1/TGFβ axis, opening new avenues for the treatment of DMD.
2021-08-30 | GSE157674 | GEO
Project description:Fibro-adipogenic progenitors (FAPs) are emerging cellular components of the skeletal muscle regenerative environment. The alternative functional phenotype of FAPs - either supportive of muscle regeneration or promoting fibro-adipogenic degeneration - is a key determinant in the pathogenesis of muscular diseases, including Duchenne Muscular Dystrophy (DMD). However, the molecular regulation of FAPs is still unknown. We show here that an "HDAC-myomiR-BAF60 variant network" regulates the functional phenotype of FAPs in dystrophic muscles of mdx mice. Combinatorial analysis of gene expression microarray and genome-wide chromatin remodeling by Nuclease accessibility (NA)-seq revealed that HDAC inhibitors de-repress a "latent" myogenic program in FAPs from dystrophic muscles at early stages of disease progression. In these cells HDAC inhibition promoted the expression of two core components of the myogenic transcriptional machinery, MyoD and BAF60C, and upregulated the myomiRs (miRs) miR-1.2, miR-133 and miR-206, which target two alternative BAF60 variants (BAF60A and B) ultimately leading to the activation of a pro-myogenic program at the expense of the fibro-adipogenic phenotype. By contrast, FAPs from dystrophic muscles at late stages of disease progression displayed resistance to HDACi-induced chromatin remodeling at myogenic loci and fail to activate the pro-myogenic phenotype. These results reveal a previously unappreciated disease stage-specific bipotency of mesenchimal cells within the regenerative environment of dystrophic muscles. Resolution of such bi-potency by epigenetic interventions, such as HDACi, provides the molecular rationale for the in situ reprogramming of target cells to promote therapeutic regeneration of dystrophic muscles. miRNA modulation upon Histone Deacetylase inhibition in Fibro-Adipogenic Progenitors (FAPs) derived from young mdx mice was evaluated by small RNA-sequencing in 2 controls and 2 treated samples
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Project description:Overloading mesenchymal progenitors (FAPs)
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Project description:Overloading mesenchymal progenitors (FAPs)
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Project description:Fibro-adipogenic progenitors (FAPs) are emerging cellular components of the skeletal muscle regenerative environment. The alternative functional phenotype of FAPs - either supportive of muscle regeneration or promoting fibro-adipogenic degeneration - is a key determinant in the pathogenesis of muscular diseases, including Duchenne Muscular Dystrophy (DMD). However, the molecular regulation of FAPs is still unknown. We show here that an "HDAC-myomiR-BAF60 variant network" regulates the functional phenotype of FAPs in dystrophic muscles of mdx mice. Combinatorial analysis of gene expression microarray and genome-wide chromatin remodeling by Nuclease accessibility (NA)-seq revealed that HDAC inhibitors de-repress a "latent" myogenic program in FAPs from dystrophic muscles at early stages of disease progression. In these cells HDAC inhibition promoted the expression of two core components of the myogenic transcriptional machinery, MyoD and BAF60C, and upregulated the myomiRs (miRs) miR-1.2, miR-133 and miR-206, which target two alternative BAF60 variants (BAF60A and B) ultimately leading to the activation of a pro-myogenic program at the expense of the fibro-adipogenic phenotype. By contrast, FAPs from dystrophic muscles at late stages of disease progression displayed resistance to HDACi-induced chromatin remodeling at myogenic loci and fail to activate the pro-myogenic phenotype. These results reveal a previously unappreciated disease stage-specific bipotency of mesenchimal cells within the regenerative environment of dystrophic muscles. Resolution of such bi-potency by epigenetic interventions, such as HDACi, provides the molecular rationale for the in situ reprogramming of target cells to promote therapeutic regeneration of dystrophic muscles.
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Project description:Skeletal muscle possesses the ability to adapt its size in response to milieus, which is called plasticity. Resistance training induces the increment of muscle mass called muscle hypertrophy. Muscle stem cells (MuSC; also known as muscle stem cells) function to supply new nuclei for myofiber during the overload in muscle. We found that Yap1 and Taz in mesenchymal progenitors (also called FAPs) are critical for MuSC proliferation in overloaded muscles. We hypothsize that Yap1/Taz-dependent mesenchymal progenitors derived factor induces MuSC proliferation. In order to identify such factors, RNA-seq of overloaded FAPs were performed.
2021-11-19 | GSE162827 | GEO
Project description:In order to understand the role of miRNAs in muscle regeneration we injected cardiotoxin into the tibialis muscle of mice and isolated using FACS two different groups of adult muscle stem cells. RNA was isolated directly from sorted cells and analyzed by miRNA deep sequencing.
2016-10-29 | E-MTAB-5177 | biostudies-arrayexpress
Project description:Skeletal muscle possesses the ability to adapt its size in response to milieus, which is called plasticity. Resistance training induces the increment of muscle mass called muscle hypertrophy. Muscle stem cells (MuSC; also known as muscle stem cells) function to supply new nuclei for myofiber during the overload in muscle. We hypothesize that mesenchymal progenitors (also called FAPs) -derived factor induces MuSC proliferation. In order to identify such factors, RNA-seq of overloaded FAPs were performed.
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Project description:The purpose of this study is to investigate how melatonin-influenced promyogenic factor secreted from fibro-adipogenic progenitors (FAPs) regulate muscle regeneration and muscle cell fusion during muscle repair. We highlighted the role of melatonin in regulating crosstalk between muscle stem cells and FAPs during muscle regeneration. Mice that were treated with melatonin exhibited improved muscle regeneration and reduced intramuscular fat deposition, which were associated with enhanced myogenesis, remodeled lipid metabolism and reduced immune cell infiltration. Notably, melatonin did not exert positive effects on cell fusion and myotube formation during differentiation. Interestingly, melatonin repressed fibro-adipogenic progenitor (FAP) adipogenesis in a dose-dependent manner in vitro. Furthermore, melatonin treatment enhanced the pro-myogenic effects of FAPs, which stimulated GDF10 secretion to promote muscle cell fusion and induce myotube hypertrophy.
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Project description:We report the bulk RNA-seq of healthy and senescent mouse fibro-adipogenic progenitors (FAPs)
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