Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA385348 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5504990.fastq.gz | Fastqsanger.gz | |||
| SRR5505000_1.fastq.gz | Fastqsanger.gz | |||
| SRR5505000_2.fastq.gz | Fastqsanger.gz | |||
| SRR5505010_1.fastq.gz | Fastqsanger.gz | |||
| SRR5505010_2.fastq.gz | Fastqsanger.gz |
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Project description:In this study, we used C3H/10T1/2 cells, a well known model of myogenic conversion, to study the effect of Six4 knockdown on the expression of genes during fibroblasts to myocytes conversion induced by ectopic expression of MyoD We established C3H/10T1/2 cell line with stable Six4 knockdown by short hairpin RNA (shSix4) vs a control cell line (shLuc) and converted these cells into myogenic lineage by retroviral transduction of plasmid encoding Flag-MyoD-myc (pBABE-MyoD) or empty plasmid (pBABE). Cells were then induced to differentiate for 24 hours before RNA extraction.
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Project description:In this study, we used C3H/10T1/2 cells, a well known model of myogenic conversion, to study the effect of Six4 knockdown on the expression of genes during fibroblasts to myocytes conversion induced by ectopic expression of MyoD
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Project description:Analysis of ex vivo isolated lymphatic endothelial cells from the dermis of patients to define type 2 diabetes-induced changes. Results preveal aberrant dermal lymphangiogenesis and provide insight into its role in the pathogenesis of persistent skin inflammation in type 2 diabetes. The ex vivo dLEC transcriptome reveals a dramatic influence of the T2D environment on multiple molecular and cellular processes, mirroring the phenotypic changes seen in T2D affected skin. The positively and negatively correlated dLEC transcripts directly cohere to prolonged inflammatory periods and reduced infectious resistance of patients´ skin. Further, lymphatic vessels might be involved in tissue remodeling processes during T2D induced skin alterations associated with impaired wound healing and altered dermal architecture. Hence, dermal lymphatic vessels might be directly associated with T2D disease promotion. Global gene expression profile of normal dermal lymphatic endothelial cells (ndLECs) compared to dermal lymphatic endothelial cells derived from type 2 diabetic patients (dLECs).Quadruplicate biological samples were analyzed from human lymphatic endothelial cells (4 x diabetic; 4 x non-diabetic). subsets: 1 disease state set (dLECs), 1 control set (ndLECs)
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Project description:Conversion of fibroblasts into skeletal muscle cells by overexpression of the transcription factor MyoD has been widely employed over past decades in a multitude of experimental settings. However, the potential of additional myogenic regulatory factors such as Myf5, Myf6 and Myog to elicit a myogenic conversion has been significantly less studied. To address this disparity, we set out to investigate the role of MRFs in fibroblast conversion into skeletal muscle stem and differentiated cells. Surprisingly, we found that Myf6, a transcription factor associated with postnatal late-stage myogenesis, efficiently converted fibroblasts into myotubes alone, or alternatively into expandable Pax7-expressing induced myogenic progenitor cells (iMPCs) in the presence of defined small molecules. To investigate reprogramming dynamics in a tightly regulated system, we generated an inducible Myf6 overexpression transgenic mouse model, which enabled dissection of transcription and epigenetic dynamics unique to iMPC formation. Mechanistically, we characterized the chromatin binding of Myf6, as well as its protein binding partners, during iMPC reprogramming and conventional transdifferentiation, revealing shared and different targets and binding partners. To further investigate its role, we surprisingly found that endogenous Myf6 is dispensable for iMPC formation by MyoD and small molecules. In accordance with this observation, we demonstrated that subjecting MyoD-KO fibroblasts to reprogramming with Myf6 and small molecules gave rise to expandable MyoD-KO iMPCs, indicating that MyoD is similarly dispensable for iMPC formation and self-renewal. Multi-omics analyses of Myf6-derived MyoD-KO iMPCs uncovered upregulated genes that compensated for the lack of MyoD, whose downregulation during iMPC production mitigated Pax7 expression, highlighting their roles as reprogramming regulators. Collectively, these results illustrate a redundancy between MRFs’ function in myogenic cellular conversions, highlighting an unexpected potency for Myf6 in the induction of a muscle stem cell fate in vitro.
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Project description:Conversion of fibroblasts into skeletal muscle cells by overexpression of the transcription factor MyoD has been widely employed over past decades in a multitude of experimental settings. However, the potential of additional myogenic regulatory factors such as Myf5, Myf6 and Myog to elicit a myogenic conversion has been significantly less studied. To address this disparity, we set out to investigate the role of MRFs in fibroblast conversion into skeletal muscle stem and differentiated cells. Surprisingly, we found that Myf6, a transcription factor associated with postnatal late-stage myogenesis, efficiently converted fibroblasts into myotubes alone, or alternatively into expandable Pax7-expressing induced myogenic progenitor cells (iMPCs) in the presence of defined small molecules. To investigate reprogramming dynamics in a tightly regulated system, we generated an inducible Myf6 overexpression transgenic mouse model, which enabled dissection of transcription and epigenetic dynamics unique to iMPC formation. Mechanistically, we characterized the chromatin binding of Myf6, as well as its protein binding partners, during iMPC reprogramming and conventional transdifferentiation, revealing shared and different targets and binding partners. To further investigate its role, we surprisingly found that endogenous Myf6 is dispensable for iMPC formation by MyoD and small molecules. In accordance with this observation, we demonstrated that subjecting MyoD-KO fibroblasts to reprogramming with Myf6 and small molecules gave rise to expandable MyoD-KO iMPCs, indicating that MyoD is similarly dispensable for iMPC formation and self-renewal. Multi-omics analyses of Myf6-derived MyoD-KO iMPCs uncovered upregulated genes that compensated for the lack of MyoD, whose downregulation during iMPC production mitigated Pax7 expression, highlighting their roles as reprogramming regulators. Collectively, these results illustrate a redundancy between MRFs’ function in myogenic cellular conversions, highlighting an unexpected potency for Myf6 in the induction of a muscle stem cell fate in vitro.
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