Ontology highlight
ABSTRACT:
PROVIDER: PRJNA590458 | ENA |
REPOSITORIES: ENA
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Project description:Dascyllus trimaculatus Genome sequencing and assembly
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Project description:Array-based comparative genomic hybridization comparing splenic marginal zone lymphoma (SMZL) specimens with control DNA
2014-01-01 | GSE34768 | GEO
Project description:Cranial sutures separate neighboring skull bones and contain skeletal stem cells that drive bone growth. A key question is how osteogenic activity is controlled to promote bone growth while preventing aberrant bone fusions during skull expansion. Here we integrate single-cell transcriptomics, in vivo expression validation, photoconversion-based lineage tracing, and a zebrafish craniosynostosis model to uncover key developmental transitions regulating bone formation during skull expansion. In addition to conservation of meninges and osteoblast lineage cells between zebrafish and mouse, single-cell transcriptomic analysis of the zebrafish skull reveals distinct subpopulations of suture mesenchyme that undergo transcriptomic changes during suture establishment. While lineage tracing with an osteoblast-specific nlsEOS reporter shows that bone formation largely occurs at suture edges, a subset of mesenchyme cells in the mid-suture region upregulate a suite of genes including BMP antagonists (e.g. grem1a) and pro-angiogenic factors. Further, lineage tracing with grem1a:nlsEOS reveals that this mid-suture subpopulation is largely non-osteogenic. In twist1b; tcf12 mutant zebrafish, a model for the coronal synostosis of Saethre-Chotzen Syndrome, reduction of grem1a+ mid-suture cells correlates with misregulated bone formation and reduced blood vessels at the coronal suture. In addition, combinatorial mutation of BMP antagonists enriched in the mid-suture subpopulation results in increased BMP signaling in the suture, misregulated bone formation, and abnormal suture morphology. These data support roles of a subset of mid-suture mesenchyme in locally promoting BMP antagonism that ensures proper suture morphology.
2024-07-11 | GSE223147 | GEO
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare NGS-derived suture transcriptome profiling (RNA-seq) among wild type, Twist1+/- and Twist1+/- with suture regeneration surgery mice Methods: Suture mRNA profiles from one week after induction of seven-month-old wild type, Twist1+/- and Twist1+/- with suture regeneration surgery mice were generated by deep sequencing, in triplicate, using Illumina NextSeq500. Results: Using an optimized data analysis workflow, we mapped about 70 million sequence reads per sample to the mouse genome ( mm10) and identified 43,644 transcripts in the suture of wild type, Twist1+/- and Twist1+/- with suture regeneration surgery mice with Partek E/M workflow.
2020-08-04 | GSE155562 | GEO
Project description:Axin2-expressing calvarial suture stem cells can contribute to calvarial development, homeostatic maintenance, repair, and regeneration. We used microarray to examine the gene expression profiles of Axin2-expressing suture stem cells and Axin2-negative cells in suture mesenchyme.
2015-11-11 | GSE74849 | GEO
Project description:Hypertrophic scars arise from dysregulated wound healing under prolonged mechanical tension, causing disfiguring fibrosis. However, limited preclinical models replicate key features of human tension-induced scarring. We developed an innovative murine model utilizing suture anchoring to impose persistent transverse-axial stretch across healing incisions, mimicking excessive wound tension that leads to hypertrophy clinically. Dorsal paired incisions were generated in mice, with wound edges on the upper back sutured to the rib cage while leaving wound edges on the lower back relaxed. This localized anchoring restrained wound contraction, maintaining high tension throughout remodeling analogous to scars widening under stress. Stretched upper wounds developed profound fibrotic changes compared to relaxed controls. Scars induced by suture-anchored tension displayed macroscopic hypertrophy, hardness, erythema, and pruritis up to 3 months. Histologically, scars induced by suture-anchored tension were hypercellular, hypervascular, hyperproliferative with disorganized extracellular matrix deposition, and displayed molecular hallmarks of hypertrophic fibrosis. MiRNA sequencing revealed the different signature in suture-anchored tension induced hypertrophic scars compared to control normal scars.
2023-09-28 | GSE243948 | GEO