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Fate determination of msc by inflammatory niche in HO [spatial transcriptomics]

ABSTRACT: Fate determination of msc by inflammatory niche in HO [spatial transcriptomics]

PROVIDER: PRJNA1032946 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26552519_1.fastq.gz	Fastqsanger.gz
	SRR26552519_2.fastq.gz	Fastqsanger.gz
	SRR26552520_1.fastq.gz	Fastqsanger.gz
	SRR26552520_2.fastq.gz	Fastqsanger.gz
	SRR26552521_1.fastq.gz	Fastqsanger.gz

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Fate determination of msc by inflammatory niche in HO

Project description:Fate determination of msc by inflammatory niche in HO

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Fate determination of msc by inflammatory niche in HO [spatial transcriptomics]

Project description:Heterotopic ossification (HO), usually following traumatic challenges, is initiated by the aberrant osteochondral differentiation of mesenchymal stem cell (MSC). However, the role of trauma-induced inflammatory exposure in MSC fate determination remains unclear. Here, we found that quiescent MSC transited into cycling MSC and later gave rise to chondrogenic (cMSC) and/or osteogenic (oMSC) commitment following either muscle or tendon injury via single-cell RNA sequencing and lineage tracing analysis. Further spatial transcriptome analysis revealed that cycling MSC, cMSC and oMSC resided in the inflammatory niche comprised of monocytes/macrophages, neutrophils, dendritic cells (DCs), NK cells, T and B lymphocytes. We uncovered the diversity of each type of immune cells during MSC development and demonstrated that macrophages, including M1 and M2 subtypes, dynamically promotes proliferation and osteochondral differentiation of MSCs. Additionally, neutrophils and NK cells are essential for cycling MSC transition from quiescent MSC. CD4+ and CD8+ T lymphocytes promotes chondrogenesis. CellchatDB analysis and regulon analysis identify several gene networks, which could be essential for aberrant MSC proliferation and osteochondral differentiation respectively. Collectively, our findings indicate that inflammation is necessary to regulate MSC fate and uncovered the molecular landscape of osteoimmunological interactions that occur during aberrant osteochondral differentiation that could be useful for HO treatment.

2025-03-06 | GSE246448 | GEO

Fate determination of msc by inflammatory niche in HO [scRNA-Seq]

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Fate determination of msc by inflammatory niche in HO [scRNA-Seq]

Project description:Fate determination of msc by inflammatory niche in HO [scRNA-Seq]

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Fate determination of msc by inflammatory niche in HO

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-03-06 | GSE246449 | GEO

Metabolic determination of cell fate through selective inheritance of mitochondria

Project description:Metabolic characteristics of adult stem cells are distinct from their differentiated progeny, and cellular metabolism is emerging as a potential driver of cell fate conversions. However, how metabolism influences fate determination remains unclear. Here, we identified inherited metabolism imposed by functionally distinct mitochondrial age-classes as a fate determinant in asymmetric division of epithelial stem-like cells. While chronologically old mitochondria support oxidative respiration, new organelles are immature and metabolically less active. Upon cell division, selectively segregated mitochondrial age-classes elicit a metabolic bias in progeny cells, with old mitochondria imposing oxidative energy metabolism inducing differentiation. High pentose phosphate pathway flux, promoting redox maintenance, is favoured in cells receiving newly synthesised mitochondria, and is required to maintain stemness during early fate determination after division. Our results demonstrate that fate decisions are susceptible to intrinsic metabolic bias imposed by selectively inherited mitochondria.

2021-12-20 | PXD010667 | Pride

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Project description:Metazoan development depends on accurate execution of differentiation programs that allow pluripotent stem cells to adopt specific fates. Differentiation is brought about by global changes to chromatin architecture and transcriptional networks, yet whether other regulatory events support cell fate determination is less well understood. Using human embryonic stem cell and Xenopus models, we identified the vertebrate-specific ubiquitin ligase Cul3KBTBD8 as an essential regulator of neural crest specification. Cul3KBTBD8 monoubiquitylates NOLC1 and its paralog TCOF1, whose mutation underlies the craniofacial disorder Treacher Collins Syndrome that is characterized by a loss of cranial neural crest cells. Ubiquitylation of NOLC1 and TCOF1 drives formation of a platform that connects RNA polymerase I with ribosome modification enzymes, thereby altering the translational program of differentiating cells to support the generation of neural crest cells. We conclude that the dynamic regulation of ribosome function is an important feature of cell fate determination. Ribosome profiling and mRNA-Seq

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