GEO 数据集

主题由标题与摘要自动归类；样本量为数据集标注之和，SuperSeries 可能与其 SubSeries 重复计算。

• RNA sequence, structure, and cell type specific features drive pseudouridylation by PUS7 [invitroBIDPool1]
  GSE314388Homo sapiens6 个样本2026-10-28

  Pseudouridines are abundant mRNA modifications that can impact splicing, translation, and stability to tune gene expression. PUS7 is one of the major mRNA pseudouridine synthases whose dysregulation leads to neurodevelopmental disorders and cancer, underscoring the critical function of PUS7-dependent pseudouridines. Beyond a short and degenerate consensus sequence, the molecular mechanisms underlying PUS7-mediated pseudouridylation remain unknown. A lack of targeted, high-throughput pseudouridine detection methods limits simultaneous interrogation of PUS7 regulatory features across many experimental conditions. We developed novel Nanopore sequencing tools, including Nano-Mod-Amp, to reveal pseudouridine stoichiometry, its RNA structural context, and dependence on PUS7 levels at specific sites across biological conditions. We established that RNA sequence and structural features are important for efficient mRNA modification by PUS7. Perturbing structure through mutations or antisense oligos modulates pseudouridylation levels. Pseudouridines are largely responsive to PUS7 protein levels, demonstrating the regulatory potential of varying PUS7 levels across cellular conditions. Conversely, PUS7 activity is also regulated in a cell-type specific manner, independent of PUS7 expression levels in a manner consistent with regulation by RNA structure and RNA binding proteins. Together, we uncovered regulatory features guiding PUS7 activity using new Nanopore sequencing tools, enabling site specific modulation of PUS7-dependent pseudouridines. Our framework can be applied to other RNA-modifying enzymes to query the regulation of the epitranscriptome.

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• RNA sequencing demonstrates alterations in the gene expression profile of HUVECs upon NETs stimulation.
  GSE314216Homo sapiens6 个样本2026-10-28

  RNA sequencing was applied to comprehensively assess changes in the gene expression profile of HUVECs following exposure to control or NETs.
• ACSS2-Mediated Metabolic-Epigenetic Crosstalk Drives Fulvestrant Resistance and Represents a Novel Therapeutic Target [NanoString]
  GSE300553Homo sapiens6 个样本2026-10-28

  Endocrine therapies target hormone-dependent cancer cells, primarily through estrogen receptor alpha (ERα), expressed in ~70% of breast cancers (ER+). Despite treatment advances, 30-40% of ER+ breast cancer patients experience recurrence and metastasis, with 5-year survival rates of only 31.9%. We validated poor outcomes for liver metastasis patients treated with Fulvestrant (Fulv) using the local Carle Foundation Hospital cohort and examined metabolic pathways in liver metastatic patient-derived xenograft (PDX) models, revealing upregulated lipid and acetyl-CoA production. Our previous work demonstrated that combining Fulv with acetyl-CoA synthase inhibitor (ACSI) targeting Acyl-CoA Synthetase Short Chain Family Member 2 (ACSS2), synergistically reduced ER+ metastatic breast cancer (MBC) cell viability in vitro. Using multiple analytical approaches—isotope tracing, CUT&RUN sequencing, immunofluorescence, western blot, and RNA sequencing—we characterized the effects of acetyl-CoA synthesis inhibition on Fulv-induced alterations. Results showed increased ACSS2 expression and acetate utilization with Fulv treatment. Isotope tracing revealed that Fulv decreased acetate flux to the TCA cycle while promoting fatty acid synthesis, though fatty acid synthesis inhibition did not synergize with Fulv. Importantly, ACSS2 was predominantly nuclear for therapy-resistant cells, suggesting epigenetic regulation roles. CUT&RUN sequencing showed Fulv treatment increased global ACSS2 binding sites and ERα/ACSS2/H3K27ac overlapping sites, which combination ACSI+Fulv therapy completely eliminated. RNA sequencing revealed increased cell proliferation gene expression with Fulv treatment. Combination therapy reduced metastatic burden. Our findings indicate ACSS2 contributes to endocrine therapy resistance through nuclear acetyl-CoA provision for epigenetic alterations. Targeting these cancer cell adaptations represents a novel therapeutic approach potentially reducing metastasis-related mortality and improving breast cancer treatment outcomes.
• Alternative splicing plays an important role in fast chemical reprogramming [scRNA-Seq]
  GSE292990Mus musculus2 个样本2026-10-28

  To investigate the role of Ptbp3 during reprogramming, scRNA-seq was carried out with RNAs isolated from the reprogramming intermediates transfected with shNC or shPtbp3.

  单细胞
• Alternative splicing plays an important role in fast chemical reprogramming [RNA-Seq]
  GSE292989Mus musculus4 个样本2026-10-28

  To investigate the role of Ptbp3 during reprogramming, deep RNA-seq was carried out with RNAs isolated from the reprogramming intermediates transfected with shNC or shPtbp3.
• Effect of stable knockdown of KRT18 on gene expression of SAS cells
  GSE292554Homo sapiens6 个样本2026-10-28

  KRT18 was reported to emerge at invasive front and was correlated to poor prognosis in oral squamous cell carcinoma. We extracted the RNA for sequencing from SAS cells which included that of wild type control groups and of stable KRT18 knockdown groups. From the results of GSEA analysis, the hallmark gene sets of epithelial mesenchymal transition (EMT) in KRT18 knockdown cells was highly suppressed. This implied that the emergence of KRT18 at invasive front of oral squamous cell carcinoma and the behavior of invasiveness of the cancer cells might be correlated to the process of EMT.
• Effect of PRAME overexpression on gene expression of A549 NSCLC cells
  GSE292191Homo sapiens4 个样本2026-10-28

  To investigate the function of PRAME in lung cancer, we established OE PRAME A549 cell line.
• OMP38 of carbapenem-resistant Acinetobacter baumannii-mediated mtDNA release activates the cGAS-STING signalling to induce inflammatory response
  GSE280491Mus musculus5 个样本2026-10-28

  Carbapenem-resistant Acinetobacter baumannii (CRAB) has become a major threat in the treatment of bacterial infection, and immunotherapy in a non-antibiotic-dependent manner is an effective way to overcome CRAB infection. However, the role of the innate immune response in CRAB infection is poorly understood. Here, we reported that CRAB infection induced a cytosolic DNA-sensing signalling pathway and significant IFN-β production in mice post CRAB infection. The knockout of STING reduced bacterial burden, the production of inflammatory cytokines and lung injury in mice post CRAB infection. The cytosolic DNA sensor cyclic GMP-AMP synthase (cGAS) and the adaptor protein stimulator of interferon genes (STING) were required for CRAB-induced IFN-β expression in macrophages. Intriguingly, CRAB utilized outer membrane vesicles (OMVs) to transport outer membrane protein 38 (OMP38) into mitochondria, triggering mitochondrial DNA (mtDNA) release into the cytosol through the mitochondrial permeability transition pore (mPTP) and activating the cGAS-STING signalling. Finally, epigallocatechin gallate (EGCG) was demonstrated to block the activation of the cGAS-STING pathway and ameliorate CRAB-induced excessive inflammatory response. These results demonstrated that the early innate immune response to CRAB infection was activated in a cGAS-STING-dependent manner, which could be a potential therapeutic target for CRAB infection.
• Filamin B, a novel RNA-binding protein, extensively regulates the expression and alternative splicing of genes associated with osteoblast development in MC3T3-E1 cells
  GSE246668Mus musculus6 个样本2026-10-28

  Filamin B (FLNB) encodes an actin-binding protein and also acts as a novel RNA-binding protein involved in cell movement and signal transduction, playing a crucial role in bone growth. However, the impact of dysregulated FLNB expression on the molecular level in the skeletal system remain unknown. In this study, stably transfected MC3T3-E1 cell lines with FLNB knockdown were constructed to investigate the regulatory mode of FLNB in the molecular level of osteoblasts by RNA-seq sequencing. Functionality experiments revealed that FLNB knockdown led to decreased proliferation, migration, and differentiation of MC3T3-E1 cells compared to the empty vector group. In addition, differentially expressed genes (DEGs) and results showed that FLNB was mainly enriched in the expression of genes related to osteoblast proliferation, differentiation and migration, such as ITGA10, Cebpβ, Grem1, etc. Alternative splicing (AS) results observed significant changes in Tpx2 and Evc related to skeletal development.According to the current study, we conducted the first investigation into the transcriptomic and alternative splicing level of FLNB in pre-osteoblast to analyze its regulatory function in bone growth and development. This study lays the foundation for the current insights into the mechanisms of gene regulation mediated by FLNB during skeletal development.
• Overexpression of desmin and vimentin in primary human bladder smooth muscle cells
  GSE127725Homo sapiens9 个样本2026-10-28

  Desmin and Vimentin overexpression differentially regulates smooth muscle gene expression in primary human bladder smooth muscle (HBSM) cells
• Transcriptome-wide mapping reveals an RNA-dependent mechanism of platinum cancer drugs. [ChIP-Seq_Spike-In]
  GSE352210Homo sapiens6 个样本2026-10-27

  Clinically used small molecules has been predicted to off-target to RNAs. However, the extend of this interaction is small molecule cancer therapeutics has not been characterized. Here, we screened for anticancer smalll molecules for their RNA interactions and uncovered widespread RNA off-targeting. Cisplatin was found to be one among the RNA binders. We used it as a model agent to identify the specific transcripts it interact with. To accomplish this, we developed Plat-RNAseq, a click-chemistry-mediated transcriptome-wide assay. Our results revealed that cisplatin binding was enriched at guanine-rich regions capable of forming RNA G-quadruplexes (rG4s) .We found that the recruitment of cisplatin to rG4s partially contributed to its cytotoxicity, revealing a noncanonical mechanism of action for this widely used chemotherapeutic agent. To assess the prevalence of RNA Pol II stalling in the cisplatin-target RNA we used RNA Pol II ChIP-seq and caculated the genome-wide stalling. This experiment uses RNA Pol II ChIP-seq with a Drosophila chromatin spike-in for quantitative normalization, unlike the previously deposited Pol II ChIP-seq (GSE309934), which was normalized to library size without a spike-in.
• GRHL2 loss alters redox homeostasis and attenuates erastin-induced ferroptosis in colorectal cancer cells
  GSE352117Homo sapiens6 个样本2026-10-27

  Redox homeostasis critically determines ferroptosis sensitivity, but the role of grainyhead-like 2 (GRHL2) in colorectal cancer remains unclear. RNA sequencing was performed to compare parental HCT116 cells with a CRISPR/Cas9-generated B8 GRHL2-KO clone and to define GRHL2-associated transcriptional changes relevant to redox homeostasis and ferroptosis sensitivity.
• Micro-C-TALE: BAC-based targeted high-resolution measurement of 3D chromatin interactions [Micro-C-TALE]
  GSE351910Homo sapiens2 个样本2026-10-27

  Chromosome conformation capture methods have greatly advanced our understanding of genome organization, but obtaining high-resolution interaction maps of selected genomic regions remains costly due to the sequencing requirements. Here, we introduce Micro-C-TALE, a new chromosome conformation capture method that combines Micro-C, which uses micrococcal nuclease to the resolution and sensitivity of chromatin interaction measurements, and C-TALE, which uses probes generated from bacterial artificial chromosomes (BACs) for targeted enrichment. This combination enables the generation of high-resolution interaction maps without requiring custom synthesis of capture oligonucleotides. We applied Micro-C-TALE to a 214 kb region in human HAP1 cells, obtaining detailed interaction maps with approximately ~5-6 million sequenced read pairs. Compared with published genome-wide Micro-C data, Micro-C-TALE yielded a higher amount of informative interactions within the targeted region despite ~550-fold lower sequencing depth. To evaluate the sensitivity of the method to fine-scale changes in genome organization, we introduced a CTCF binding site into the targeted region using CRISPR-Cas9. Comparing Micro-C-TALE to the restriction enzyme-based C-TALE, we found Micro-C yielded a ~5-fold higher fraction of informative reads and detected novel CTCF-mediated point interactions associated with the inserted CTCF site, which were barely discernible using C-TALE. Our results demonstrate that Micro-C-TALE provides a flexible and cost-effective approach for targeted high-resolution measurement of chromatin interactions, facilitating the investigation of fine-scale genome organization and its response to genetic perturbations.

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• Micro-C-TALE: BAC-based targeted high-resolution measurement of 3D chromatin interactions [C-TALE]
  GSE351909Homo sapiens1 个样本2026-10-27

  Chromosome conformation capture methods have greatly advanced our understanding of genome organization, but obtaining high-resolution interaction maps of selected genomic regions remains costly due to the sequencing requirements. Here, we introduce Micro-C-TALE, a new chromosome conformation capture method that combines Micro-C, which uses micrococcal nuclease to the resolution and sensitivity of chromatin interaction measurements, and C-TALE, which uses probes generated from bacterial artificial chromosomes (BACs) for targeted enrichment. This combination enables the generation of high-resolution interaction maps without requiring custom synthesis of capture oligonucleotides. We applied Micro-C-TALE to a 214 kb region in human HAP1 cells, obtaining detailed interaction maps with approximately ~5-6 million sequenced read pairs. Compared with published genome-wide Micro-C data, Micro-C-TALE yielded a higher amount of informative interactions within the targeted region despite ~550-fold lower sequencing depth. To evaluate the sensitivity of the method to fine-scale changes in genome organization, we introduced a CTCF binding site into the targeted region using CRISPR-Cas9. Comparing Micro-C-TALE to the restriction enzyme-based C-TALE, we found Micro-C yielded a ~5-fold higher fraction of informative reads and detected novel CTCF-mediated point interactions associated with the inserted CTCF site, which were barely discernible using C-TALE. Our results demonstrate that Micro-C-TALE provides a flexible and cost-effective approach for targeted high-resolution measurement of chromatin interactions, facilitating the investigation of fine-scale genome organization and its response to genetic perturbations.

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• SB89: A Murine Dermis-Derived Macrophage Cell Line for Studies of Skin Immune Responses
  GSE351881Mus musculus6 个样本2026-10-27

  Resident dermal macrophages (DMs) play essential roles in maintaining skin homeostasis and initiating inflammatory responses during tissue injury and against infectious agents. However, studies of their cellular mechanisms have been limited by their low abundance in steady-state skin and by technical challenges in isolating resident DMs. Here, we describe the generation and characterization of a novel DM cell line, termed SB89. F4/80+ skin-resident DMs were sorted and immortalized using J2 retroviral transduction. SB89 cells display a stable, homogeneous macrophage phenotype and distinct surface markers compared with Langerhans cells and alveolar macrophages. Functionally, SB89 cells efficiently phagocytose methicillin-resistant Staphylococcus aureus (MRSA), Escherichia coli, zymosan particles, and apoptotic cells, and effectively kill MRSA. Importantly, SB89 cells respond to LPS, as evidenced by production of IL-6, TNF, and Nos2, and by MRSA-induced production of inflammatory cytokines, chemokines, and eicosanoids. Importantly, SB89 cells are genetically tractable and amenable to genetic manipulation, supporting efficient miRNA gene silencing via RNAi and gene introduction via plasmid-based gene expression transfection. Bulk RNA-seq analysis revealed that SB89 cells are transcriptionally distinct from immortalized bone marrow-derived macrophages and are enriched for pathways associated with innate immune responses, chemotaxis, cell adhesion, and GPCR signaling. Together, these findings establish SB89 as a renewable, genetically tractable dermis-derived macrophage model that can support reproducible studies of skin-associated macrophage functions. This cell line represents a powerful platform for mechanistic, genetic, and translational studies in skin immunobiology.
• Spatial transcriptomic profiling of human left ventricular tissue in ischaemic heart disease and dilated cardiomyopathy
  GSE351778Homo sapiens2 个样本2026-10-27

  Spatially resolved single-cell gene expression profiling was performed on fresh-frozen human left ventricular tissue from one ischaemic heart disease (IHD) and one dilated cardiomyopathy (DCM) specimen. The Xenium Human Multi-Tissue and Cancer Gene Expression panel supplemented with 100 custom probes was used to characterise cardiomyocytes and cardiac fibroblasts and investigate spatial relationships between fibroblast subpopulations and cardiomyocyte.

  单细胞空间转录组
• Adipose mitochondrial functional enhancement via DsbA-L rewires systemic aging through an adipokine-mediated longevity pathway
  GSE351767Mus musculus4 个样本2026-10-27

  Mitochondrial dysfunction is a hallmark of aging, but whether restoring mitochondrial function in adipose tissue alone can delay systemic aging is unknown. Here we show that adipose-specific upregulation of the mitochondrial chaperone DsbA-L in mice improves metabolic and cognitive function and extends lifespan, linking adipose mitochondrial fitness directly to systemic aging. DsbA-L upregulation reprograms adipose gene expression and raises circulating levels of the adipokine Serpina3m. Fat-body-specific knockdown of Spn42De (CG9460), the Drosophila serpin counterpart of Serpina3m, shortens lifespan, whereas its overexpression extends it. SERPINA3, the human ortholog, is enriched in centenarians. Unlike conventional mitochondrial enhancers, DsbA-L couples metabolic efficiency to endocrine signaling, and berberine increases DsbA-L expression, indicating that this pathway is pharmacologically tractable. These benefits occur in both sexes and identify DsbA-L–Serpina3m signaling as a target for healthy aging.
• Transcriptomic profiling of mouse bone marrow neutrophils treated with Propionibacterium acnes with or without human umbilical cord blood mesenchymal stem cell-derived exosomes
  GSE351531Mus musculus8 个样本2026-10-27

  This study investigates transcriptional responses of mouse bone marrow neutrophils to human umbilical cord blood mesenchymal stem cell-derived exosomes during Propionibacterium acnes stimulation. Bulk RNA sequencing was performed on neutrophils exposed to P. acnes alone or to P. acnes together with exosomes. The dataset comprises eight samples and includes paired-end sequencing reads, gene-level read counts, and FPKM expression values. It supports investigation of inflammatory responses and pathways associated with neutrophil extracellular trap formation.
• Study of LETT@MVs‑induced ferroptosis in tumor cells via supplementation of PUFA
  GSE351467Homo sapiens4 个样本2026-10-27

  Ferroptosis represents a promising therapeutic strategy for cancer, yet its anti‑tumor efficacy is largely limited by insufficient polyunsaturated fatty acids (PUFA) within the tumor microenvironment (TME). Aloe vera thylakoid membranes, naturally rich in PUFA, are an ideal source to facilitate robust lipid peroxidation. To address biological delivery obstacles, we constructed tumor‑targeting biomimetic microvesicles (LETT@MVs) by engineering aloe‑thylakoid‑derived microvesicles (TDMVs) with the multifunctional peptide LETT, which enables tumor‑targeted delivery and lysosomal escape. We systematically characterized the influences of LETT@MVs on hepatocellular carcinoma (HCC) cells, including cell viability, vasculogenic mimicry (VM) formation, lipid peroxidation and ferroptosis in vitro. Antitumor potency and biosafety were further validated using an orthotopic HCC mouse model. Mechanistically, multi‑omics strategies combining bulk RNA‑seq, metabolomics and scRNA‑seq were applied to decipher underlying molecular events. LETT@MVs were effectively internalized by HCC cells and successfully escaped lysosomal degradation. Taking advantage of endogenous PUFA stored in thylakoid components, LETT@MVs triggered potent lipid peroxidation and ferroptosis, meanwhile remodelled the extracellular matrix (ECM) to suppress vasculogenic mimicry. In orthotopic HCC mice, LETT@MVs markedly retarded tumor growth via ferroptosis induction and VM repression without obvious safety risks. Integrated multi‑omics data demonstrated that LETT@MVs rewired transcriptional and metabolic profiles of HCC cells, driving highly‑metabolic tumor cells toward ferroptotic stress status and generating near‑death cell subpopulations. Collectively, our work validates that aloe‑thylakoid‑originated biomimetic nanoplatform can trigger robust tumor ferroptosis through PUFA supplementation, providing new clues to conquer ferroptosis resistance and advance therapeutic interventions for hyper‑metabolic tumors.

  单细胞
• Microglial lipid signaling drives glioblastoma invasion and represents a therapeutic vulnerability
  GSE348401Mus musculus8 个样本2026-10-27

  Glioblastoma (GBM) is characterized by diffuse infiltration into the surrounding brain, limiting complete surgical resection, the strongest determinant of patient survival. The mechanisms driving this invasive growth remain incompletely understood. Here, we identify a lipid-mediated paracrine signaling axis through which tumor-associated microglia/macrophages promote glioma invasion. Integrating single-cell transcriptomics, spatial lipidomics, and functional perturbation across mouse models and human GBM samples, we show that invading tumor cells engage and reprogram myeloid cells via CSF1R–PI3K signaling. This induces lipid metabolic reprogramming and secretion of bioactive lipids, including lysophosphatidylcholines (LPCs) and lysophosphatidic acids (LPAs), which promote GBM invasion through distinct downstream pathways. Disruption of this myeloid–GBM axis, reduces lipid secretion and suppresses invasion. Targeting downstream LPA–LPAR or YAP/TAZ signaling further constrains invasion in a context-dependent manner. Together, these findings define a lipid-driven circuit linking the tumor microenvironment to glioma invasion and identify strategies to reduce infiltration and improve surgical resection.

  单细胞空间转录组扰动筛选
• Glioma regulates GABAergic signaling to drive hyperactivity and tumor progression [RNA-seq]
  GSE348105Mus musculus6 个样本2026-10-27

  Recent studies identified bi-directional communication between neurons and glioma tumors as a key driver of hyperexcitability and malignant progression. While much of this work has focused on the activity of excitatory neurons, roles for inhibitory neurons remain poorly defined. Using in-vivo screening approaches in autochthonous glioma models, we found that loss of a GABA transporter (Slc6a1) enhanced glioma progression, promoted network hyperactivity, and influenced tonic GABA release by tumors. Mechanistically, we show that glioma tumors influence the activity of inhibitory neurons and their subsequent stimulation suppresses tumor growth. Further screening of these phenomena identified Diazepam Binding Inhibitory (DBI), a secreted negative allosteric modulator of GABA-A, as a link between glioma related hyperexcitability and proliferation that functions through modulating inhibitory neuronal signaling. Collectively, our findings indicate that glioma tumors utilize multiple mechanisms to manipulate the activity of inhibitory neurons as a means to drive network hyperactivity, which ultimately facilitates malignant progression.
• Glioma regulates GABAergic signaling to drive hyperactivity and tumor progression
  GSE348034Mus musculus4 个样本2026-10-27

  Recent studies identified bi-directional communication between neurons and glioma tumors as a key driver of hyperexcitability and malignant progression. While much of this work has focused on the activity of excitatory neurons, roles for inhibitory neurons remain poorly defined. Using in-vivo screening approaches in autochthonous glioma models, we found that loss of a GABA transporter (Slc6a1) enhanced glioma progression, promoted network hyperactivity, and influenced tonic GABA release by tumors. Mechanistically, we show that glioma tumors influence the activity of inhibitory neurons and their subsequent stimulation suppresses tumor growth. Further screening of these phenomena identified Diazepam Binding Inhibitory (DBI), a secreted negative allosteric modulator of GABA-A, as a link between glioma related hyperexcitability and proliferation that functions through modulating inhibitory neuronal signaling. Collectively, our findings indicate that glioma tumors utilize multiple mechanisms to manipulate the activity of inhibitory neurons as a means to drive network hyperactivity, which ultimately facilitates malignant progression.
• ScRNA-seq reveals cellular heterogeneity in urethral stricture
  GSE347480Homo sapiens6 个样本2026-10-27

  Urethral strictures are characterized by fibrotic scar tissue formation in the urethra, leading to difficulties in urination and potential renal dysfunction. The cellular microenvironment contributes to stenosis. However, the heterogeneity of key cell types hinders our understanding of this disease. Single-cell RNA sequencing was performed on three urethral scar tissues and three normal urethral tissues. First, the main cell types and sample heterogeneity were identified. Transcription factor (TF) and enrichment analyses were used to characterize the transcriptional regulation and metabolic patterns of fibroblasts and mast cells. Finally, CellChat was used to elucidate intercellular communication networks in urethral scar tissues. Of the eight cell types detected, fibroblasts, mast cells, and macrophages were major contributors to urethral scar tissue. These cells were categorized into seven (FB0–FB6), two (Mast0 and Mast1), and nine (Macro0-Macro8) subclusters, respectively, based on heterogeneity. Urethral scar tissue exhibited increased proportions of FB3 fibroblast, Mast1 mast cell, Macro1, and Macro7 counts. Marker genes of these subclusters facilitated the dysregulation of fibrosis through various biological processes, including cell adhesion and extracellular matrix organization. Additionally, screening of the dysregulation of multiple TFs and metabolic pathways revealed potential candidate TFs—ETS1 (from FB3) and SMAD3 (from Mast1)—associated with fibrosis. Furthermore, communication substantially increased between fibroblasts and other cells, and between Macro1 or Macro7 and other macrophage subclusters or fibroblasts in urethral scar tissue. We revealed the transcriptional characteristics of key cells involved in the fibrogenesis of urethral stricture, which elucidates the pathogenesis of urethral stenosis and advances the exploration of therapeutic targets.

  单细胞
• Molecular Imaging of the TGF-β Activating Integrin avb6 Detects Chronic Lung Allograft Dysfunction
  GSE346597Mus musculus2 个样本2026-10-27

  TGF-β-activating integrins promote solid-organ fibrosis, suggesting their potential as disease markers. Chronic lung allograft dysfunction (CLAD), a progressive fibrotic complication that limits lung transplant survival, is driven by intragraft TGF-β activation. However, TGF-β-activating integrin expression patterns remain undefined in lung transplants. Single-cell RNA sequencing and proteomic analysis of tissue specimens from a mouse CLAD model and human explanted lungs with CLAD revealed high levels of the TGF-β-activating integrin αvβ6, primarily localized to fibrosis-associated Keratin 8+ alveolar transitional epithelial cells, which were greatly reduced in tolerant lungs. Molecular imaging with a newly optimized positron emission tomography radiotracer specific for avb6, [64Cu]Cu-DOTA-A20-K16R, showed significantly higher uptake in CLAD than in tolerant transplants. [64Cu]Cu-DOTA-A20-K16R activity was also reduced by experimental treatments that lowered avb6 expression and inhibited CLAD severity. Finally, [64Cu]Cu-DOTA-A20-K16R autoradiographic analysis of human explanted lungs with CLAD showed elevated activity that correlated with increased avb6 expression. Collectively, these findings illustrate the potential utility of αvβ6 molecular imaging for detecting CLAD pathogenesis.

  单细胞
• YS-10 Exerts Therapeutic Effects on Radiation-Induced Testicular Damage
  GSE345816Rattus norvegicus9 个样本2026-10-27

  This study comparatively analyzed RNA‑sequencing data of rat testicular tissues from the control group, radiation‑induced injury model group, and treatment group
• Single-cell profiling of microglia transcriptomes transduced by the AAV-MSRE tool
  GSE345675Mus musculus9 个样本2026-10-27

  This study profiles the transcriptomic responses of microglia transduced with the AAV-MSRE tool at single-cell resolution. Single-cell RNA sequencing was used to characterize transduced microglial populations, assess their molecular identities, and evaluate transcriptional changes associated with AAV-MSRE delivery. These data provide a resource for examining the cellular specificity and transcriptomic impact of AAV-MSRE-mediated targeting in microglia.

  单细胞
• Transcriptomic profiling of M1-like and M2-like mouse bone marrow-derived macrophages
  GSE344431Mus musculus6 个样本2026-10-27

  Macrophage activation states are involved in intestinal inflammation and tissue remodeling, but the transcriptional programs linking macrophage polarization to ulcerative colitis-associated molecular changes remain incompletely characterized. In this study, primary bone marrow-derived macrophages from mice were polarized toward M1-like or M2-like states and subjected to bulk RNA sequencing. M1-like polarization was induced using lipopolysaccharide and interferon-gamma, whereas M2-like polarization was induced using interleukin-4 and interleukin-13. Three biological replicates were analyzed per group. The resulting transcriptomes were used to identify macrophage polarization-related genes and were subsequently integrated with ulcerative colitis macrophage single-cell transcriptomic and circulating proteomic evidence to prioritize disease-associated macrophage candidates.

  单细胞
• Hi-C analysis of HCT-116 and K562 cells
  GSE339260Homo sapiens2 个样本2026-10-27

  We performed Hi-C analysis on two common cancer cell lines.
• A single cell atlas defines perinatal factors that drive murine bone marrow development
  GSE318094Mus musculus2 个样本2026-10-27

  Processes that direct initial colonization and maturation of the bone marrow remain elusive, despite their importance to lifelong hematopoiesis. Bone marrow mesenchymal and stromal cell (BMSC) maturation must establish supportive hematopoietic niches prior to the recruitment and colonization of hematopoietic stem cells (HSCs). Here, we define the identity of murine BMSC progenitors and temporal nature of marrow colonization through a single cell atlas spanning late gestation through 18 months of age. We define progenitor cells and developmental trajectories for Cxcl12-abundant reticular (CAR) cells and osteoblasts within the marrow, including the emergence of direct and secreted signaling modalities that impact HSC quiescence and regenerative capacity. We further identify temporal changes in Early B Cell Factor (Ebf) 1-3 transcription factor expression and activity that correlate with niche establishment. These transcriptional activities relate to change to changes in systemic physiology, including metabolic, inflammatory, and hypoxic signaling, that direct CAR cell emergence after birth in mice. These findings provide unprecedented resolution to the colonization and maturation of the murine bone marrow environment.

  单细胞细胞图谱
• CEBPA-Induced Trophectoderm-like Cells from Pluripotent Stem Cells Enable Modeling of Trophoblast Lineage Specification [scRNA-Seq]
  GSE315752Mus musculus1 个样本2026-10-27

  Trophoblast lineages are essential for placental development and play indispensable roles in mammalian development. However, the regulatory mechanisms governing trophoblast lineage specification, particularly trophectoderm formation, remain elusive. Here, we show that transient overexpression of the transcription factor Cebpa in mouse pluripotent stem cells efficiently generates trophectoderm-like cells that recapitulate key transcriptional features of trophectoderm. These trophectoderm-like cells can be further induced to form trophoblast organoids and exhibit developmental competence to generate all trophoblast lineages in vitro. Mechanistically, Cebpa overexpression drives extensive epigenetic reprogramming toward a trophectoderm-like state, including global remodeling of chromatin accessibility and coordinated changes in H3K4me3 and H3K27me3 histone modifications. CUT&RUN analyses further reveal binding of CEBPA to multiple trophectoderm-specific enhancers. Together, our findings identify Cebpa as a potent inducer of trophectoderm potential and establish a new platform for modeling trophectoderm lineage specification in vitro.

  单细胞