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Assessment of myogenic maturation for human iPSC-derived iPAX7 myogenic progenitors in vitro and in vivo

ABSTRACT: Assessment of myogenic maturation for human iPSC-derived iPAX7 myogenic progenitors in vitro and in vivo

PROVIDER: PRJNA1023472 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26264681_1.fastq.gz	Fastqsanger.gz
	SRR26264681_2.fastq.gz	Fastqsanger.gz
	SRR26264682_1.fastq.gz	Fastqsanger.gz
	SRR26264682_2.fastq.gz	Fastqsanger.gz
	SRR26264683_1.fastq.gz	Fastqsanger.gz

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Assessment of myogenic maturation for human iPSC-derived iPAX7 myogenic progenitors in vitro and in vivo

Project description:Here, we transplanted human iPAX7 myogenic progenitors into skeletal muscles of non-dystrophic and dystrophic mice and compared the transcriptional landscape of human donor-derived myofibers with respective in vitro-differentiated iPAX7 myotubes. Pairing bulk RNA sequencing with computational deconvolution of human reads, we were able to pinpoint key myogenic changes that occur during the in vitro-to-in vivo transition, confirm developmental maturity, and consequently further suggest the utility of cell-based therapies.

2024-04-02 | GSE244521 | GEO

Cellular and transcriptomic changes by the supplementation of aged rat serum in human pluripotent stem cell-derived myogenic progenitors

Project description:Introduction: The changing composition of non-cell autonomous circulating factors in blood as humans age is believed to play a role in muscle mass and strength loss. The mechanisms through which these circulating factors act in age-related skeletal muscle changes is not fully understood. In this study, we used human myogenic progenitors derived from human pluripotent stem cells to study non-cell autonomous roles of circulating factors during the process of myogenic differentiation. Methods: Myogenic progenitors from human embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs) were supplemented with serum samples from aged or young Fischer 344 × Brown Norway F1-hybrid rats. The effect of aged or young serum supplementation on myogenic progenitor proliferation, myotube formation capacity, differentiation, and early transcriptomic profiles were analyzed. Results: We found that aged rat serum supplementation significantly reduced cell proliferation and increased cell death in both ESC- and iPSC-derived myogenic progenitors. Next, we found that the supplementation of aged rat serum inhibited myotube formation and maturation during terminal differentiation from progenitors to skeletal myocytes when compared to the cells treated with young adult rat serum. Lastly, we identified that gene expression profiles were affected following serum supplementation in culture. Discussion: Together, aged serum supplementation caused cellular and transcriptomic changes in human myogenic progenitors. The current data from our in vitro model possibly simulate non-cell autonomous contributions of blood composition to age-related processes in human skeletal muscle.

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human iPSC-derived thyroid follicular cells maturation depends on time and duration of BMP-signaling

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PAX3-FOXO1 dictates myogenic reprogramming and rhabdomyosarcoma identity in endothelial progenitors [RNA-seq]

Project description:Fusion-positive rhabdomyosarcoma (FP-RMS) driven by the expression of the PAX3-FOXO1 (P3F) fusion oncoprotein is an aggressive subtype of pediatric rhabdomyosarcoma. FP-RMS histologically resembles developing muscle yet occurs throughout the body in areas devoid of skeletal muscle highlighting that FP-RMS is not derived from an exclusively myogenic cell of origin. Here we demonstrate that P3F reprograms mouse and human endothelial progenitors to FP-RMS. We show that P3F expression in aP2-Cre expressing cells reprograms endothelial progenitors to functional myogenic stem cells capable of regenerating injured muscle fibers. Further, we describe a FP-RMS mouse model driven by P3F expression and Cdkn2a loss in endothelial cells. Additionally, we show that P3F expression in TP53-null human iPSCs blocks endothelial-directed differentiation and guides cells to become myogenic cells that form FP-RMS tumors in immunocompromised mice. Together these findings demonstrate that FP-RMS can originate from aberrant development of non-myogenic cells driven by P3F.

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