Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA283532 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2016031_1.fastq.gz | Fastqsanger.gz | |||
| SRR2016031_2.fastq.gz | Fastqsanger.gz | |||
| SRR2016032_1.fastq.gz | Fastqsanger.gz | |||
| SRR2016032_2.fastq.gz | Fastqsanger.gz | |||
| SRR2016033_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
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Project description:In response to skeletal muscle injury, adult myogenic stem cells, known as satellite cells, are activated and undergo proliferation and differentiation to regenerate new muscle fibers. The skeletal muscle-specific microRNA, miR-206, is up-regulated in satellite cells following muscle injury, but its role in muscle regeneration has not been defined. Here we show that skeletal muscle regeneration in response to cardiotoxin injury is impaired in mice lacking miR-206. Loss of miR-206 also accelerates and exacerbates the dystrophic phenotype of mdx mice, a model for Duchenne muscular dystrophy. MiR-206 promotes satellite cell differentiation and fusion to form multinucleated myofibers by suppressing a collection of negative regulators of myogenesis. Our findings reveal an essential role for miR-206 in satellite cell differentiation during skeletal muscle regeneration and as a modulator of Duchenne muscular dystrophy. total RNA obtained from TA muscle of mdx and 3 miR-206 KO; mdx mice at 3 months of age.
2012-04-30 | E-GEOD-36077 | biostudies-arrayexpress
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:MicroRNAs (miRNAs) are important in the regulation of many biological processes including muscle development. However, little is known regarding miRNA regulation of muscle regeneration. In mature murine tibialis anterior muscle following injury, 298 miRNAs were significantly changed during the time course of muscle regeneration including 86 that were altered greater than 10-fold as compared to uninjured muscle. Temporal miRNA expression patterns were identified and included inflammation-related miRNAs (miR-223 and -147) that increased immediately after injury; this pattern contrasted to that of mature muscle-specific miRNAs (miR-1, -133a and -499) that were abruptly decreased following injury and then up-regulated in later regenerative events. Another cluster of miRNAs were transiently increased in the early days of muscle regeneration. This included miR-351, a miRNA that was also transiently expressed during myogenic progenitor cell (MPC) differentiation in vitro. Based on computational predictions, further studies demonstrated that E2f3 was a target of miR-351 in myoblasts. Moreover, knockdown of miR-351 expression inhibited MPC proliferation and promoted apoptosis during MPC differentiation, whereas miR-351 overexpression protected MPC from apoptosis during differentiation. Collectively, these observations suggest that miR-351 is involved in both the maintenance of MPC proliferation and the transition of MPC into differentiated myotubes. Thus, a novel, time-dependent sequence of molecular events during skeletal muscle regeneration has been identified, i.e., miR-351 inhibits E2f3 expression, a key regulator of cell cycle progression and proliferation, and promotes MPC proliferation and protects early differentiating MPC from apoptosis, important events in the hostile tissue environment after acute muscle injury. Skeletal muscles are damaged and repaired repeatedly throughout life. Muscle regeneration maintains locomotor function during aging and delays the appearance of clinical symptoms in neuromuscular diseases, such as Duchenne muscular dystrophy. The capacity for skeletal muscle growth and regeneration is conferred by satellite cells located between the basal lamina and the sarcolemma of mature myofibers. Upon injury, satellite cells reenter the cell cycle, proliferate, and then exit the cell cycle either to renew the quiescent satellite cell pool or to differentiate into mature myofibers. Despite recent advances, genes involved in these processes are still largely unknown. Understanding the molecular mechanisms that regulate satellite cell activities could promote development of novel countermeasures to enhance muscle regeneration that is compromised by diseases or aging. Using a muscle injury mouse model, we profiled miRNA expression during muscle regeneration.
2012-04-24 | E-GEOD-37479 | biostudies-arrayexpress
Project description:Following skeletal muscle injury, muscle stem cells (satellite cells) are activated, proliferate, and differentiate to form myofibers. We show that mRNA decay protein AUF1 regulates satellite cell function through targeted degradation of specific mRNAs. AUF1 targets certain mRNAs containing 3 AU-rich elements (AREs) for rapid decay. Auf1-/- (KO) mice undergo accelerated skeletal muscle wasting with age and impaired muscle repair following injury. Satellite cell mRNA analysis and regeneration studies demonstrate that auf1-/- satellite cell self-renewal is impaired due to increased stability and overexpression of ARE-mRNAs. Control of ARE-mRNA decay by AUF1 and potentially other ARE-binding proteins represents a mechanism for adult stem cell regulation and is implicated in human muscle wasting diseases. We report the RNA transcript expression profiles from sorted satellite cells isolated from wild type (WT) and AUF1-null (KO) mice hindlimb muscles Examination of RNA transcript expression from satellite cells of two genotypes Please note that mice are bred through a C57BL/6 strain of 129 background.
2016-07-21 | E-GEOD-83555 | biostudies-arrayexpress
Project description:In response to skeletal muscle injury, adult myogenic stem cells, known as satellite cells, are activated and undergo proliferation and differentiation to regenerate new muscle fibers. The skeletal muscle-specific microRNA, miR-206, is up-regulated in satellite cells following muscle injury, but its role in muscle regeneration has not been defined. Here we show that skeletal muscle regeneration in response to cardiotoxin injury is impaired in mice lacking miR-206. Loss of miR-206 also accelerates and exacerbates the dystrophic phenotype of mdx mice, a model for Duchenne muscular dystrophy. MiR-206 promotes satellite cell differentiation and fusion to form multinucleated myofibers by suppressing a collection of negative regulators of myogenesis. Our findings reveal an essential role for miR-206 in satellite cell differentiation during skeletal muscle regeneration and as a modulator of Duchenne muscular dystrophy.
2012-05-01 | GSE36077 | GEO
Project description:Long non-coding RNAs (lncRNAs) are family of gene regulators but the functional study of lncRNAs in skeletal muscle satellite cells (SCs) remains at the infancy stage. Here we identify SAM (Sugt1 associated muscle) lncRNA (also known as Snhg15, (small nucleolar RNA host gene 15) that is enriched in the proliferating myoblast cells and down-regulated as the cells progressed to differentiation. Gain- or loss- of function of SAM in muscle SCs alters myogenic proliferation and differentiation. Global deletion of SAM based on the KO-first strategy has no overt effect on mice but impairs adult muscle regeneration following acute damage; the loss also exacerbates the chronic injury induced dystrophic phenotype in the mdx mouse model. Consistently, inducible deletion of SAM in adult SCs leads to deficiency in acute injury-induced muscle regeneration. Further examination of SCs revealed that SAM loss results in cell autonomous defect in proliferative expansion of myoblasts. Mechanistically, we find SAM interacts and stabilizes Sugt1 (suppressor of G2 allele of SKP1) protein, a co-chaperon protein key to kinetochore assembly during cell division. Loss of SAM or Sugt1 both cause disruptive kinetochore assembly and microtubule attachment in mitotic cells due to mis-localization of key components Dsn1 and Hec1 proteins. Altogether, our findings identify SAM as a regulator of SC proliferation through facilitating Sugt1 mediated kinetochore assembly during cell division.
2020-05-18 | PXD018147 | Pride
Project description:Adult muscle stem cells (satellite cells) are required for adult skeletal muscle regeneration. A proper balance between quiescence, proliferation, and differentiation is essential for the maintenance of the satellite cell pool and their regenerative function. Although the ubiquitin-proteasome is required for most protein degradation in mammalian cells, how its dysfunction affects tissue stem cells remains unclear. Here, we investigated the function of the proteasome in satellite cells using mice lacking the crucial proteasomal component, Rpt3. Ablation of Rpt3 in satellite cells decreased proteasome activity. Proteasome dysfunction in Rpt3-deficient satellite cells impaired their ability to proliferate, survive and differentiate, resulting in defective muscle regeneration. We found that inactivation of proteasomal activity induced proliferation defects and apoptosis in satellite cells. Mechanistically, insufficient proteasomal activity upregulated the p53 pathway, which caused cell-cycle arrest. Our findings delineate a critical function of the proteasome system in maintaining satellite cells in adult muscle.
2018-10-10 | GSE114354 | GEO
Project description:Skeletal muscle has remarkable capacity to regenerate upon injury due to the presence of satellite cells. The maintenance and function of satellite cells are regulated by circadian clock. Cryptocrhome 2 (CRY2) is a key component of the circadian clock and its role in skeletal muscle regeneration remains controversial. Here, we report that CRY2 is down-regulated during muscle regeneration. Using the satellite cell specific CRY2 knockout mice (CRY2scko), we show that deletion of CRY2 enhances muscle regeneration. Single myofiber analysis showed that deletion of CRY2 enhances satellite cell self-renewal. In the absence of CRY2, the ERK1/2 and JNK1/2 signaling pathways become activated, which phosphorylates the transcription factor ETS1, which in turn binds to the promoter of PAX7 to induce its transcription. CRY2 deficient myoblasts survived better in ischemic muscle. Deletion of CRY2 also alleviated myopathy in mdx mice. Therefore, CRY2 plays an essential role in regulating satellite cell function and skeletal muscle regeneration.
2024-04-07 | GSE171651 | GEO
Project description:Following skeletal muscle injury, muscle stem cells (satellite cells) are activated, proliferate, and differentiate to form myofibers. We show that mRNA decay protein AUF1 regulates satellite cell function through targeted degradation of specific mRNAs. AUF1 targets certain mRNAs containing 3 AU-rich elements (AREs) for rapid decay. Auf1-/- (KO) mice undergo accelerated skeletal muscle wasting with age and impaired muscle repair following injury. Satellite cell mRNA analysis and regeneration studies demonstrate that auf1-/- satellite cell self-renewal is impaired due to increased stability and overexpression of ARE-mRNAs. Control of ARE-mRNA decay by AUF1 and potentially other ARE-binding proteins represents a mechanism for adult stem cell regulation and is implicated in human muscle wasting diseases. We report the RNA transcript expression profiles from sorted satellite cells isolated from wild type (WT) and AUF1-null (KO) mice hindlimb muscles
2016-07-21 | GSE83555 | GEO
Project description:Satellite cells are the primary source of stem cells for skeletal muscle growth and regeneration. Since adult stem cell maintenance involves a fine balance between intrinsic and extrinsic mechanisms, we performed genome-wide chronological expression profiling to identify the transcriptomic changes involved during early postnatal growth till acquisition of satellite cell quiescence.
2015-04-21 | GSE65927 | GEO