Identification of chemically-induced osteogenic cells (ciOG) through single cell RNA-seq
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ABSTRACT:
PROVIDER: PRJNA849341 | ENA |
REPOSITORIES: ENA
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Project description:Chemically-induced osteogenic cells (ciOG)
| PRJNA849336 | ENA
Project description:Here we report the reprogramming of human fibroblasts to produce chemically-induced osteogenic cells (ciOG), and explore the potential uses of ciOG in bone repair and disease treatment. A chemical cocktail of RepSox, forskolin, and phenamil was used for osteogenic induction of fibroblasts by activation of RUNX2 expression. Following a maturation, the cells differentiated toward an osteoblast phenotype that produced mineralized tissue. Single-cell RNA sequencing analysis of ciOG identified unique clusters of cells, among which the cluster of active cells related to osteogenic cells was ~49% of the cells, or ~80% of active cells; another cluster of active cells (~12% of the cells) was related to fibroblasts. The reprogramming trajectory over time revealed the transition from fibroblasts to mainly osteogenic cells or to an inactive state.
2022-09-15 | GSE206138 | GEO
Project description:Chemically-induced osteogenic cells (ciOG) from fibroblasts
| PRJNA849333 | ENA
Project description:Here we report the reprogramming of human fibroblasts to produce chemically-induced osteogenic cells (ciOG), and explore the potential uses of ciOG in bone repair and disease treatment. A chemical cocktail of RepSox, forskolin, and phenamil was used for osteogenic induction of fibroblasts by activation of RUNX2 expression. Following a maturation, the cells differentiated toward an osteoblast phenotype that produced mineralized tissue. Bulk RNA sequencing revealed that up- and down-regulated genes in ciOG relative to aHDF resembled those in hOB during maturation.
2022-09-15 | GSE206136 | GEO
Project description:Here we report the reprogramming of human fibroblasts to produce chemically-induced osteogenic cells (ciOG), and explore the potential uses of ciOG in bone repair and disease treatment. A chemical cocktail of RepSox, forskolin, and phenamil was used for osteogenic induction of fibroblasts by activation of RUNX2 expression. Following a maturation, the cells differentiated toward an osteoblast phenotype that produced mineralized tissue. When generated on a nanofiber substrate ciOG accelerated osteogenic gene expressions and mineralization compared to PCL film followed by bone matrix formation in a calvarial defect, indicating that the engineered biomaterial promotes the osteogenic capacity of ciOG in vivo.
2022-09-15 | GSE206137 | GEO
Project description:Chemically-induced osteogenic cells (ciOG) in PCL (polycarprolactone) film and NF (nanofiber)
| PRJNA849342 | ENA
Project description:Generation of chemically induced totipotent cells through multi-parametric analysis of single-cells
| PRJNA516696 | ENA
Project description:Developmental exposure to environmental toxicants is a cause of skeletal abnormalities. Yet the molecular mechanisms linking early exposure to impaired bone formation remain undefined. Skeletal tissues arise from both neural crest- and mesoderm-derived lineages that rely on shared osteogenic differentiation programs, suggesting that disruption of common regulatory processes may contribute to diverse skeletal outcomes. MicroRNAs (miRNAs) are key post-transcriptional regulators of gene networks and have appeared as indicators of toxicant-induced perturbation. In this study, we examined whether developmentally relevant toxicants are associated with miRNA regulatory networks during osteogenic differentiation. Using a human embryonic stem cell (hESC)-based osteogenic differentiation model, we assessed the effects of nine toxicants spanning distinct primary mechanisms. Toxicant exposure impaired osteogenic differentiation at their IC50, as reflected by altered expression of osteogenic markers and transcriptional remodeling. Global miRNA profiling revealed dysregulation of miRNAs enriched for bone-related biological processes, including regulators of osteogenic commitment and differentiation timing. Integrated miRNA–mRNA network analysis identified a subset of miRNAs linked to core osteogenic and lineage-associated pathways, including RUNX2-dependent transcription and BMP and Wnt signaling. Modulation of representative miRNAs produced osteogenic outcomes consistent with those observed following toxicant exposure and, in some cases, was associated with partial restoration of differentiation in exposed cultures. Collectively, these findings indicate that chemically diverse developmental toxicants are associated with miRNA-mediated regulatory patterns during osteogenic differentiation. Identification of conserved miRNA signatures provides mechanistic insight into developmental bone toxicity and supports the use of miRNA network analysis as a human-relevant endpoint for skeletal hazard identification.
2026-05-31 | GSE324490 | GEO
Project description:Pluripotent stem cells fluctuate among distinct functional cell states. Such heterogeneity undermines the potential applications of stem cells in regenerative medicine. The heterogeneity of pluripotent cell states and their molecular nature remain less understood. Here, we utilized mass cytometry to dissect pluripotent cell states by simultaneously profiling multiple proteins and their modifications in single cells. Results indicated the role of extensive signaling cross-talk among multiple pathways in regulating cell state heterogeneity. By systematically dissecting the signals and their combinations, we identify conditions through which large portions of pluripotent cells can be chemically reprogrammed into totipotent cells which can be cultured. Unlike pluripotent cells, these chemically induced totipotent cells (CiTC) give rise to both embryonic and extra-embryonic cell types. In addition, CiTCs are molecularly distinct from pluripotent cells. CiTCs provide an in-vitro model to understand the nature of totipotent cells and the plasticity of pluripotent cells. Our quantitative and integrative approach provides general method to understand similar heterogenous cell systems such as cancer.
2024-03-01 | GSE125536 | GEO
Project description:Developmental exposure to environmental toxicants is a cause of skeletal abnormalities. Yet the molecular mechanisms linking early exposure to impaired bone formation remain undefined. Skeletal tissues arise from both neural crest- and mesoderm-derived lineages that rely on shared osteogenic differentiation programs, suggesting that disruption of common regulatory processes may contribute to diverse skeletal outcomes. MicroRNAs (miRNAs) are key post-transcriptional regulators of gene networks and have appeared as indicators of toxicant-induced perturbation. In this study, we examined whether developmentally relevant toxicants are associated with miRNA regulatory networks during osteogenic differentiation. Using a human embryonic stem cell (hESC)-based osteogenic differentiation model, we assessed the effects of nine toxicants spanning distinct primary mechanisms. Toxicant exposure impaired osteogenic differentiation at their IC50, as reflected by altered expression of osteogenic markers and transcriptional remodeling. Global miRNA profiling revealed dysregulation of miRNAs enriched for bone-related biological processes, including regulators of osteogenic commitment and differentiation timing. Integrated miRNA–mRNA network analysis identified a subset of miRNAs linked to core osteogenic and lineage-associated pathways, including RUNX2-dependent transcription and BMP and Wnt signaling. Modulation of representative miRNAs produced osteogenic outcomes consistent with those observed following toxicant exposure and, in some cases, was associated with partial restoration of differentiation in exposed cultures. Collectively, these findings indicate that chemically diverse developmental toxicants are associated with miRNA-mediated regulatory patterns during osteogenic differentiation. Identification of conserved miRNA signatures provides mechanistic insight into developmental bone toxicity and supports the use of miRNA network analysis as a human-relevant endpoint for skeletal hazard identification.
2026-05-31 | GSE324491 | GEO