Ontology highlight
ABSTRACT:
PROVIDER: PRJNA281047 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Identification of post-transcriptional regulatory networks during myeloblast-to-monocyte differentiation transition [mRNA]
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Project description:Identification of post-transcriptional regulatory networks during myeloblast-to-monocyte differentiation transition [miRNA]
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Project description:Ischemic stroke promotes monocyte recruitment to the injured brain and their differentiation into monocyte-derived macrophages (MDMs). These cells contribute to debris clearance but may also exacerbate neuroinflammation. However, the heterogeneity of macrophage subsets and the phenotypic transitions that shape MDM functional states during the subacute phase of stroke remain incompletely characterized. To address this, we first performed single-cell RNA sequencing (scRNA-seq) to define the transcriptional landscape of the mouse brain 48 hours after transient middle cerebral artery occlusion/reperfusion compared with sham controls. Reclustering of macrophage-lineage cells identified multiple monocyte-derived subsets, including a distinct Cd68hi/Ctsdhi MDM subset enriched for lysosomal and lipid-processing gene expression programs. Cell trajectory inference supported a transition from inflammatory infiltrates toward the Cd68hi/Ctsdhi state, accompanied by induction of transcriptomic networks that drive macrophage function to favor a clearance-competent phenotype in response to ischemic stroke. Complementary single-cell ATAC sequencing (scATAC-seq) demonstrated cell type-specific chromatin remodeling after stroke and revealed MDM subclusters with accessibility at key loci regulating lysosomal function and lipid metabolism. Together, our findings define a cellular and regulatory framework of the subacute post-stroke brain and identify a lysosome-enriched Cd68hi/Ctsdhi MDM trajectory, highlighting endolysosomal and lipid-processing programs during early stroke recovery.
2026-05-15 | GSE326118 | 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 | GSE324490 | GEO
Project description:Ischemic stroke promotes monocyte recruitment to the injured brain and their differentiation into monocyte-derived macrophages (MDMs). These cells contribute to debris clearance but may also exacerbate neuroinflammation. However, the heterogeneity of macrophage subsets and the phenotypic transitions that shape MDM functional states during the subacute phase of stroke remain incompletely characterized. To address this, we first performed single-cell RNA sequencing (scRNA-seq) to define the transcriptional landscape of the mouse brain 48 hours after transient middle cerebral artery occlusion/reperfusion compared with sham controls. Reclustering of macrophage-lineage cells identified multiple monocyte-derived subsets, including a distinct Cd68hi/Ctsdhi MDM subset enriched for lysosomal and lipid-processing gene expression programs. Cell trajectory inference supported a transition from inflammatory infiltrates toward the Cd68hi/Ctsdhi state, accompanied by induction of transcriptomic networks that drive macrophage function to favor a clearance-competent phenotype in response to ischemic stroke. Complementary single-cell ATAC sequencing (scATAC-seq) demonstrated cell type-specific chromatin remodeling after stroke and revealed MDM subclusters with accessibility at key loci regulating lysosomal function and lipid metabolism. Together, our findings define a cellular and regulatory framework of the subacute post-stroke brain and identify a lysosome-enriched Cd68hi/Ctsdhi MDM trajectory, highlighting endolysosomal and lipid-processing programs during early stroke recovery.
2026-05-15 | GSE326241 | GEO
Project description:<p>This integrated multi-omics resource delineates the molecular and phenotypic trajectories underlying male morphotype differentiation (Blue Claw [BC], Orange Claw [OC], Small Male [SM]) in <em>macrobrachium rosenbergii</em> during determinative developmental stages (100, 110, and 120 days post-stocking). The dataset comprises paired testicular transcriptomic profiles, hemolymph serum metabolomes, and quantitative morphological trait data (15 key metrics), thereby establishing a holistic framework capturing concurrent gene expression dynamics, metabolic flux alterations, and phenotypic manifestations throughout morphotype specification. The synergistic integration of these multidimensional layers enables mechanistic dissection of regulatory networks governing crustacean growth polymorphism, facilitates identification of heritable biomarkers associated with commercially advantageous morphotypes, and provides foundational insights into arthropod phenotypic plasticity.</p>
2025-08-22 | MTBLS12876 | MetaboLights
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
Project description:The transition of embryonic stem cells (ESCs) from pluripotency to lineage commitment involves complex regulatory mechanisms, including chromatin dynamics and transcriptional/post- transcriptional processes. These mechanisms often interact within intricate networks that require thorough investigation. In this study, we highlight the critical role of the mouse RNA-binding protein LIN28A in neuronal differentiation. LIN28A mediates RNA-dependent interactions with thePolycomb repressive complex 2 (PRC2), leading to the eviction of PRC2 from chromatin andactivation of a neuronal lineage-specific transcriptional program. Proteomic analyses revealed thatthe LIN28A interactome undergoes substantial remodeling during differentiation, corresponding to changes in LIN28A localization. In undifferentiated ESCs, LIN28A primarily resides in the nucleus,interacting with PRC2 components in an RNA-dependent manner, assisting in chromatin dynamics. The absence of LIN28A results in persistent PRC2 association with chromatin, impairing theexpression of genes critical for neuronal differentiation. Chromatin immunoprecipitationsequencing further confirmed that loss of LIN28A results in preferential PRC2 occupancy at thepromoters of differentiation-associated genes. These findings reveal a novel role of LIN28A inepigenetic remodeling, crucial for proper neuronal differentiation of ESCs.
2026-05-01 | GSE306869 | GEO
Project description:Advances in cellular reprogramming and stem cell differentiation now enable ex vivo studies of human neuronal differentiation. However, it remains challenging to elucidate the underlying regulatory programs because differentiation protocols are laborious and often result in low neuron yields. Here, we overexpressed two murine Neurogenin transcription factors in human induced pluripotent stem cells, and obtained neurons with bipolar morphology in four days at greater than 90% purity. The high purity enabled mRNA and microRNA expression profiling during neurogenesis, thus revealing the genetic programs involved in the transition from stem cell to neuron. These profiles were then analyzed to identify the regulatory networks underlying the differentiation of the neurons. Paired end RNA sequencing of iPS cells (PGP1) at 0, 1, 3, and 4 days post- doxycycline induction of murine NGN1 and NGN2. This was done using an Illumina HiSeq, and reads were aligned to hg19
2014-09-29 | E-GEOD-60548 | biostudies-arrayexpress