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Single-cell RNA sequencing of primary cultures of neonatal digit amputation wound cells 4 days post-amputation and treated with FGF2 for 24H

ABSTRACT: Primary wound cells were isolated and treated with FGF2 (100 ng/ml) for 24 hours, and analyzed by single cell RNA sequencing (scRNAseq). The dataset from FGF2 treated wound fibroblasts was compared to our previously published dataset for un-treated primary wound cells(GSE185197) to determine the transcriptomic changes in treated fibroblasts. We found Hmga1 and Hmga2 as novel FGF2-inducible genes potentially linked to fibroblast dedifferentiation during FGF2 induced blastema formation.

ORGANISM(S): Mus musculus

PROVIDER: GSE297901 | GEO | 2026/03/11

REPOSITORIES: GEO

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Project description:Tumor microenvironment contains various components including cancer cells, tumor vessels, and cancer associated fibroblasts (CAFs), comprising of tumor-promoting myofibroblasts and tumor-suppressing fibroblasts. Multiple lines of evidence indicated that transforming growth factor-β (TGF-β) induces the formation of myofibroblasts and other types of mesenchymal (non-myofibroblastic) cells from endothelial cells. Recent reports showed that fibroblast growth factor 2 (FGF2) modulates TGF-β-induced mesenchymal transition of endothelial cells, but the molecular mechanisms regarding the signals that control the transcriptional networks during the formation of different groups of fibroblasts remain largely unclear. Here, we studied the roles of FGF2 during the regulation of TGF-β-induced mesenchymal transition of tumor endothelial cells (TECs). We demonstrated that auto/paracrine FGF signals in TECs inhibit TGF-β-induced endothelial-to-myofibroblast transition (End-MyoT), leading to suppressed formation of contractile myofibroblast cells, but on the other hand can also collaborate with TGF-β in promoting the formation of active fibroblastic cells which have migratory and proliferative properties. FGF2 modulated TGF-β-induced formation of myofibroblastic and non-myofibroblastic cells from TECs via transcriptional regulation of the array of various mesenchymal markers and growth factors. Furthermore, we observed that TECs treated with TGF-β were more competent in promoting in vivo tumor growth than TECs treated with TGF-β and FGF2. Mechanistically, we showed that Elk1 mediated this FGF2-induced inhibition of End-MyoT via inhibition of TGF-β-induced transcriptional activation of α-SMA promoter by myocardin-related transcription factor (MRTF)-A. Our data suggest that TGF-β and FGF2 oppose and cooperate with each other during the formation of myofibroblastic and non-myofibroblastic cells from TECs to determine the characteristics of the mesenchymal cells in tumor microenvironment. Identification of marker genes for TGF-β-induced endothelial-to-myofibroblast transition

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Single-cell RNA sequencing of primary cultures of neonatal digit amputation wound cells 4 days post-amputation and treated with FGF2 for 24H

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