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Contractile fibroblasts form a transient niche for the branching mammary epithelium (unsorted cells)

ABSTRACT: Contractile fibroblasts form a transient niche for the branching mammary epithelium (unsorted cells)

PROVIDER: PRJEB91032 | ENA |

REPOSITORIES: ENA

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Contractile fibroblasts form a transient niche for the branching mammary epithelium (fibroblasts)

Project description:Contractile fibroblasts form a transient niche for the branching mammary epithelium (fibroblasts)

| PRJEB91116 | ENA

Contractile fibroblasts form a transient niche for the branching mammary epithelium (unsorted cells)

Project description:Single-cell RNA-seq of microdissected regions of pubertal mouse mammary gland, all cell types. The microdissected regions contained either terminal end buds with their surrounding stroma (\"TEB\" sample), or mature ducts with their surrounding stroma (\"duct\" sample). The animals were 5 weeks old females and each sample was pooled from 8 animals.

2025-08-07 | E-MTAB-15259 | biostudies-arrayexpress

Contractile fibroblasts form a transient niche for the branching mammary epithelium.

Project description: Not available

| S-EPMC12480840 | biostudies-literature

Contractile fibroblasts form a transient niche for the branching mammary epithelium (fibroblasts)

Project description:Single-cell RNA-seq of fibroblasts, FACS-sorted from microdissected regions of pubertal mouse mammary gland. The microdissected regions contained either terminal end buds with their surrounding stroma (\"TEB\" sample), or mature ducts with their surrounding stroma (\"duct\" sample). The animals were 5 weeks old females and each sample was pooled from 11 animals.

2025-08-07 | E-MTAB-15262 | biostudies-arrayexpress

Haloplasma contractile

Project description:Haloplasma contractile overview

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Bulk RNA-sequencing of unsorted and PAX7::GFP-sorted ESC-derived myogenic progenitors

Project description:Tissue engineering strategies that combine human pluripotent stem cell-derived myogenic progenitors (hPDMs) with advanced biomaterials provide promising tools for engineering 3D skeletal muscle grafts to model tissue development in vitro and promote muscle regeneration in vivo. We recently demonstrated (i) the potential for obtaining large numbers of hPDMs using a combination of two small molecules and (ii) the application of electrospun fibrin microfiber bundles for functional skeletal muscle restoration following volumetric muscle loss. In this study, we demonstrate that the biophysical cues provided by the microfiber bundles can induce unsorted hPDMs to form multinucleated myotubes that express desmin and myosin heavy chain. To reduce the batch-to-batch variability of these samples, we tested a genetic PAX7 reporter line (PAX7::GFP) to sort for more homogenous populations of hPDMs. RNA sequencing and gene set enrichment analyses confirmed that PAX7::GFP-sorted hPDMs exhibited higher expression of myogenic genes while unsorted hPDMs demonstrated increased expression of genes associated with embryonic, neural crest, and fibroadipogenic progenitor lineages. We tested engineered skeletal muscle grafts derived from either PAX7::GFP-sorted or unsorted hPDMs within in vivo skeletal muscle defects. The unsorted hPDM-derived grafts also exhibited greater fibrosis and more proinflammatory responses. In contrast, the PAX7::GFP-sorted groups had moderately high vascular infiltration, more implanted cell association with embryonic myosin heavy chain (eMHC) regions, and greater CD206:CD86 ratios compared to unsorted hPDMs and acellular fibers suggesting they induced more pro-regenerative microenvironments. These findings demonstrated some promise for the use of PAX7::GFP-sorted hPDMS on fibrin microfiber bundles and provided some insights for improving the cell-biomaterial system to stimulate more robust in vivo skeletal muscle regeneration.

2022-12-09 | GSE178784 | GEO

Haloplasma contractile SSD-17B

Project description:Haloplasma contractile SSD-17B genome sequencing

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Blood vessels restrain pancreas branching, differentiation and growth

Project description:How organ size and form are controlled during development is a major question of biology. Blood vessels have been shown to be essential for early development of the liver and pancreas, and are fundamental to normal and pathological tissue growth. Here we report that non-nutritional signals from blood vessels surprisingly act to restrain pancreas growth. Elimination of endothelial cells increases the size of embryonic pancreatic buds. Conversely, VEGF-induced hypervascularization decreases pancreas size. The growth phenotype results from vascular restriction of pancreatic tip cell formation, lateral branching and differentiation of the pancreatic epithelium into endocrine and acinar cells. The effects are seen both in vivo and ex vivo, indicating a perfusion-independent mechanism. Thus the vasculature controls pancreas morphogenesis and growth by reducing branching and differentiation of primitive epithelial cells.

2011-09-14 | GSE32098 | GEO

Erysiphe necator strain:branching

Project description:Erysiphe necator Genome sequencing branching isolate

| PRJNA248900 | ENA

Sonic hedgehog signaling promotes basal epidermal fibrillin 3 expression for zebrafish fin ray branching

Project description:Zebrafish robustly regenerate amputated fins, including restoring branched bony ray skeletons. During fin outgrowth, sonic hedgehog a (shha)-expressing basal epidermal cells (bEps) signal to themselves and adjacent progenitor osteoblasts (pObs) to progressively split pObs into daughter ray pools. Collectively moving bEps pass through a shha-expressing state to define distal shha-positive bEp domains that themselves separate laterally ahead of ray branching. As such, Shh/Smo signaling may promote transient associations between bEps and pObs that gradually splits pOb pools. We used bulk RNA sequencing of caudal fin regenerates after Smoothened (Smo) inhibition followed by a crispant screen to identify fibrillin 3 (fbn3) as a candidate Shh/Smo target gene for ray branching. Homozygous fbn3 mutant zebrafish regenerated caudal fins with fewer branched rays and increased distances to branch points. Shh/Smo signaling was required specifically for fbn3 induction in bEps but not pObs. Double homozygous mutants showed that fibrillin 2 (fbn2; FBN2 ortholog) redundantly supports fbn3-promoted ray branching. Fbn1-containing microfibrils accumulated at the bEp/pOb interface in fbn3 and, more so, fbn3/2 mutant regenerating caudal fins. Shh/Smo signaling may activate bEp fbn3 expression to locally modify microfibril structure and/or abundance, facilitating bEp-pOb interactions and/or movements underlying ray branching morphogenesis.

2026-01-05 | GSE312774 | GEO

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