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。

• Bulk RNA-seq profiling of regulatory and effector T cells of C57BL/6 mice
  GSE350087Mus musculus12 个样本2026-10-28

  Regulatory T cells (Tregs) maintain immune tolerance, whereas effector T cells (Teffs) mediate immune responses. Imbalance between Tregs and Teffs may contribute to immune dysregulation in type 1 diabetes mellitus (T1DM). Here, we performed bulk RNA sequencing of splenic Tregs and Teffs from control and streptozotocin-induced diabetic C57BL/6 mice to characterize disease-associated transcriptional alterations. Tregs in T1DM exhibited enhanced proliferative, effector-associated, and metabolic transcriptional programs, alongside reduced expression of genes involved in immunoregulation, lineage maintenance, tissue homing, metabolic fitness, and stress adaptation. Meanwhile, Teffs adopted a hyperactivated, but functionally imbalanced transcriptional state characterized by enhanced proliferative and inflammatory programs alongside dysregulated metabolic, signaling, and migratory functions. This study identified transcriptional alterations of splenic Tregs and Teffs in control and STZ-induced diabetic C57BL/6 mice, providing candidate molecular markers for further investigation of T-cell dysregulation in T1DM.
• Furan fatty acids reprogram hepatic lipid metabolism via acyl-CoA conjugates in obesity.
  GSE347256Mus musculus24 个样本2026-10-28

  Dietary fish oil (FO) and omega-3 fatty acids are associated with cardiometabolic benefits, yet their molecular mediators remain incompletely defined. Furan fatty acids (FuFAs), a distinct lipid class enriched in FO, have emerged as potential regulators of metabolic health. Here, we identify and quantify FuFA species in prescription omega-3 formulations and natural fish oils, and synthesize structurally engineered analogs designed to isolate antioxidant activity and β-oxidation susceptibility from FuFA bioactivity. In a diet-induced obesity mouse model, both natural and synthetic FuFAs reduced fat accumulation and inflammatory markers, while 11U3-2M additionally produce significant improvement in glucose tolerance, dyslipidemia, and hepatic steatosis. The superior activity of 11U3-2M reflects the stable accumulation of its acyl-CoA conjugate that activates peroxisome proliferator-activated receptor alpha (PPARα) signaling and allosterically inhibits acetyl-CoA carboxylases (ACCs) to reprogram hepatic lipid metabolism. These findings position FuFAs as functional dietary lipids contributing to fish oil’s metabolic effects and define fatty acid structural determinants that govern hepatic metabolic activity.
• Transcriptomic Analysis Identifies Candidate Molecular Mechanisms Underlying SCF+G-CSF-Reduced Neuropathology in Aged APP/PS1 Mice
  GSE345694Mus musculus8 个样本2026-10-28

  Alzheimer’s disease (AD) is characterized by amyloid pathology, neuroinflammation, and cognitive decline. Our previous studies demonstrated that combined treatment with stem cell factor (SCF) and granulocyte colony-stimulating factor (G-CSF) reduces AD pathology in APP/PS1 mice. In this study, we performed transcriptomic analysis to investigate candidate molecular mechanisms underlying the effects of SCF+G-CSF in aged APP/PS1 mice. Aged APP/PS1 mice received daily subcutaneous injections of SCF+G-CSF or vehicle for 12 days, and age-matched wild-type mice served as controls. Gene-chip analysis identified 27 differentially expressed genes in SCF+G-CSF-treated versus vehicle-treated APP/PS1 mice and 89 differentially expressed genes in APP/PS1 versus wild-type mice. The findings identify treatment-associated transcriptional changes involving immune regulation, metal ion homeostasis, and other molecular pathways potentially relevant to AD pathology.
• Time-resolved RNA-seq reveals a phased transcriptional response to TGFβ stimulation
  GSE343789Mus musculus40 个样本2026-10-28

  Fibroblast differentiation into matrix-producing, contractile myofibroblasts is accompanied by metabolic reprogramming, but whether these changes precede differentiation or arise from the activated phenotype remains unclear. To define when transcriptional remodeling emerges after TGFβ stimulation, we performed bulk RNA-seq on cardiac fibroblasts treated with TGFβ or bFGF for 1, 6, 12, 24, or 48 h. Our transcripomics revealed only 394 genes were differentially expressed at 1 h, but 4,188 DEGs were detected by 6 h, with the total DEG burden peaking at 24 h. These findings support a phased, time-dependent remodeling of the cardiac fibroblast transcriptome in response to TGFβ relative to bFGF in which an initially limited response occurs at 1 h, expands substantially by 6 h, and subsequently encompasses cell cycle regulation, stress responses, developmental- and differentiation-associated programs, cell adhesion, and extracellular matrix remodeling.
• Real-world river water organic pollutant mixture induces ovarian hyperandrogenism via aryl hydrocarbon receptor activation [follicular]
  GSE343593Mus musculus10 个样本2026-10-28

  Humans are exposed to complex mixtures of endocrine-disrupting chemicals (EDCs) in the real world. Most prior studies, however, focus on individual EDCs. Here, we investigated the ovarian impact of organic pollutant mixtures extracted from the Raritan River, a heavily industrialized watershed in central New Jersey, using a three-dimensional (3D) in vitro ovarian follicle culture system. Ultra-high-performance liquid chromatography-high-resolution mass spectrometry (UHPLC-HRMS) identified organic pollutant mixtures dominated by alkylphenols, pharmaceuticals, per- and polyfluoroalkyl substances (PFAS), and phthalates, together with previous reports demonstrating that the Raritan River also contains hydrophobic persistent organic pollutants (POPs), including polycyclic aromatic hydrocarbons (PAHs), polychlorinated biphenyls (PCBs), and dioxins. In vitro exposure to the Raritan River-derived EDC mixture did not affect follicle growth and ovulation but dose-dependently increased preovulatory testosterone secretion while suppressing postovulatory progesterone production. Transcriptomic analysis, Gene set enrichment analysis (GSEA), reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and in situ RNA hybridization revealed widespread reprogramming of follicular somatic cell gene expression, including altered steroidogenic pathways and activation of aryl hydrocarbon receptor (AhR) signaling. An established AhR agonist, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), reproduced the phenotype of EDC mixture-induced hyperandrogenism, which was reversed by a selective AhR inhibitor. Together, this study demonstrates that real-world EDC mixtures, particularly AhR-activating chemicals, disrupt ovarian steroidogenesis and induce hyperandrogenism, highlighting EDC mixtures as an underrecognized mechanism linking aquatic pollution to impaired women’s reproductive health.
• Real-world river water organic pollutant mixture induces ovarian hyperandrogenism via aryl hydrocarbon receptor activation
  GSE343592Mus musculus9 个样本2026-10-28

  Humans are exposed to complex mixtures of endocrine-disrupting chemicals (EDCs) in the real world. Most prior studies, however, focus on individual EDCs. Here, we investigated the ovarian impact of organic pollutant mixtures extracted from the Raritan River, a heavily industrialized watershed in central New Jersey, using a three-dimensional (3D) in vitro ovarian follicle culture system. Ultra-high-performance liquid chromatography-high-resolution mass spectrometry (UHPLC-HRMS) identified organic pollutant mixtures dominated by alkylphenols, pharmaceuticals, per- and polyfluoroalkyl substances (PFAS), and phthalates, together with previous reports demonstrating that the Raritan River also contains hydrophobic persistent organic pollutants (POPs), including polycyclic aromatic hydrocarbons (PAHs), polychlorinated biphenyls (PCBs), and dioxins. In vitro exposure to the Raritan River-derived EDC mixture did not affect follicle growth and ovulation but dose-dependently increased preovulatory testosterone secretion while suppressing postovulatory progesterone production. Transcriptomic analysis, Gene set enrichment analysis (GSEA), reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and in situ RNA hybridization revealed widespread reprogramming of follicular somatic cell gene expression, including altered steroidogenic pathways and activation of aryl hydrocarbon receptor (AhR) signaling. An established AhR agonist, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), reproduced the phenotype of EDC mixture-induced hyperandrogenism, which was reversed by a selective AhR inhibitor. Together, this study demonstrates that real-world EDC mixtures, particularly AhR-activating chemicals, disrupt ovarian steroidogenesis and induce hyperandrogenism, highlighting EDC mixtures as an underrecognized mechanism linking aquatic pollution to impaired women’s reproductive health.
• Glutamine Metabolism as a Rheostat of CD4+ T cell Pathogenic Function in Metabolic Dysfunction-Associated Steatotic Liver Disease
  GSE341871Mus musculus7 个样本2026-10-28

  Metabolic dysfunction-associated steatotic liver disease (MASLD) severity is independently linked with pathogenic CD4+ T cell responses and skewed hepatic glutamine (Gln) metabolism. Whether these processes interact to drive disease progression remains unclear. Here, we identify hepatic Gln depletion as a key feature of steatohepatitis that is linked with increased hepatic CD4+ T cell inflammation and hepatocellular damage in humans. In complementary mouse models, both total hepatic and hepatic CD4+ T cell Gln levels were similarly reduced. Restoration of hepatic Gln through supplementation selectively restrained hepatic CD4+ T cell inflammatory programs and alleviated hepatocellular damage and disease severity. Mechanistically, T cell-intrinsic Gls1-mediated glutaminolysis limited O-GlcNAcylation to dampen pathogenic CD4+ T cell inflammation. Importantly, Gln treatment dampened CD4+ T cell-mediated injury in human liver organoids. Together, these findings establish hepatic CD4+ T cell-intrinsic Gln metabolism as a critical rheostat of pathogenic inflammation in MASLD and invoke metabolism-targeted strategies to restrict disease progression.
• Immune landscape and intercellular crosstalk in the cornea of an autoimmune-mediated dry eye disease
  GSE333335Mus musculus2 个样本2026-10-28

  We have employed a single cell sequencing approach using 10x genomis scRNAseq to study the immune composition in autoimmune induced dry eye cornea. This study found a diverse immune cell composition, including T cells, B cells, neutrophils and macrophages. Moreover, we characterized cell signaling communication networks between immune and epithelial and stormal cells.

  单细胞
• mRNA and miRNA Sequencing Identifies Increased Oxidative Stress Pathways in a Mouse Model of Ethanol Exacerbation of Colitis [mRNA Seq]
  GSE329642Mus musculus24 个样本2026-10-28

  Alcohol consumption has been found to worsen the pathology of colitis. To elucidate the underlying mechanism, we performed both miRNA and mRNA sequencing of the large intestinal epithelial cells derived from a murine model of alcohol and colitis. Male C57BL/6 received Dextran Sulfate Sodium (DSS) for 5 days to induce colitis and gavaged with alcohol (~3g/kg) or water for 3 days. Three hours after the final gavage, the mice were euthanized and colon lengths were measured, followed by epithelial cell isolation. RNA, including miRNA, was isolated from the colonic epithelial cells and sent to Novogene for mRNA and miRNA sequencing. Analysis comparing DSS Ethanol vs Sham Vehicle mice showed 3931 significantly upregulated genes and 3788 significantly downregulated genes. Functional enrichment analysis of GO and KEGG pathways showed enrichment of superoxide anion generation and HIF-1 signaling pathways, both related to oxidative stress. DSS Ethanol compared to DSS Vehicle resulted in 921 significantly upregulated and 1072 significantly downregulated genes (Padj<0.05) with functional enrichment analysis showing the term with the highest fold enrichment was superoxide anion generation. We further confirmed the RNA and protein expression of NOS2, CYBB, and NCF1 which are involved in nitric oxide and superoxide production. miRNA sequencing revealed 84 differentially expressed miRNAs comparing DSS Ethanol to DSS Vehicle. Functional enrichment analysis of predicted targets of these miRNAs also showed enrichment in superoxide anion generation. These results suggest that combined ethanol and DSS exposure may increase the production of reactive oxygen species, which further damages the intestinal lining and potentially contributes to the ethanol exacerbation of colitis
• mRNA and miRNA Sequencing Identifies Increased Oxidative Stress Pathways in a Mouse Model of Ethanol Exacerbation of Colitis
  GSE329630Mus musculus23 个样本2026-10-28

  Alcohol consumption has been found to worsen the pathology of colitis. To elucidate the underlying mechanism, we performed both miRNA and mRNA sequencing of the large intestinal epithelial cells derived from a murine model of alcohol and colitis. Male C57BL/6 received Dextran Sulfate Sodium (DSS) for 5 days to induce colitis and gavaged with alcohol (~3g/kg) or water for 3 days. Three hours after the final gavage, the mice were euthanized and colon lengths were measured, followed by epithelial cell isolation. RNA, including miRNA, was isolated from the colonic epithelial cells and sent to Novogene for mRNA and miRNA sequencing. Analysis comparing DSS Ethanol vs Sham Vehicle mice showed 3931 significantly upregulated genes and 3788 significantly downregulated genes. Functional enrichment analysis of GO and KEGG pathways showed enrichment of superoxide anion generation and HIF-1 signaling pathways, both related to oxidative stress. DSS Ethanol compared to DSS Vehicle resulted in 921 significantly upregulated and 1072 significantly downregulated genes (Padj<0.05) with functional enrichment analysis showing the term with the highest fold enrichment was superoxide anion generation. We further confirmed the RNA and protein expression of NOS2, CYBB, and NCF1 which are involved in nitric oxide and superoxide production. miRNA sequencing revealed 84 differentially expressed miRNAs comparing DSS Ethanol to DSS Vehicle. Functional enrichment analysis of predicted targets of these miRNAs also showed enrichment in superoxide anion generation. These results suggest that combined ethanol and DSS exposure may increase the production of reactive oxygen species, which further damages the intestinal lining and potentially contributes to the ethanol exacerbation of colitis
• The Circadian Clock controls Hepatic Inflammation in Metabolic dysfunction-Associated Steatotic Liver Disease (MASLD) [Multi-omics]
  GSE327440Mus musculus6 个样本2026-10-28

  The circadian clock dictates time-of-day dependent gene, protein expression, and metabolite levels to ensure liver homeostasis. Circadian misalignment is implicated in the development of various metabolic disorders, but its contribution to the progression of Metabolic dysfunction-Associated Steatotic Liver Disease (MASLD) toward Metabolic dysfunction-Associated Steatohepatitis (MASH) remains poorly understood. Here, we aimed to dissect the role of the circadian clock in MASH development. Using an environmental model of chronic circadian misalignment, combined with metabolic and immune phenotyping, single nuclei transcriptomics and lipidomic profiling, we investigated the role of the clock in MASLD development and hepatic inflammation. To dissect the specific contribution of the immune clock, we used a genetic model overexpressing the clock component Rev-erbα in myeloid cells. Chronic circadian misalignment combined with a high-fat, high-sucrose, cholesterol-enriched (HFHSC) diet markedly amplified hepatic inflammation, characterized by the upregulation of pro-inflammatory genes and increased immune cell infiltration, including the expansion of lipid-associated macrophages (LAMs). Although circadian misalignment did not worsen glucose intolerance or hepatic steatosis, it altered hepatic metabolic gene expression, reflecting a broad reprogramming of immune and metabolic pathways. The circadian clock controls both FA profile and inflammatory process, and its misalignment aggravates MASLD by increasing liver inflammation. Targeting circadian regulators such as Rev-erbα in myeloid cells may offer a promising therapeutic avenue for controlling liver inflammation in MASLD.

  多组学
• The Circadian Clock controls Hepatic Inflammation in Metabolic dysfunction-Associated Steatotic Liver Disease (MASLD)
  GSE326584Mus musculus24 个样本2026-10-28

  The circadian clock dictates time-of-day dependent gene, protein expression, and metabolite levels to ensure liver homeostasis. Circadian misalignment is implicated in the development of various metabolic disorders, but its contribution to the progression of Metabolic dysfunction-Associated Steatotic Liver Disease (MASLD) toward Metabolic dysfunction-Associated Steatohepatitis (MASH) remains poorly understood. Here, we aimed to dissect the role of the circadian clock in MASH development. Using an environmental model of chronic circadian misalignment, combined with metabolic and immune phenotyping, single nuclei transcriptomics and lipidomic profiling, we investigated the role of the clock in MASLD development and hepatic inflammation. To dissect the specific contribution of the immune clock, we used a genetic model overexpressing the clock component Rev-erbα in myeloid cells. Chronic circadian misalignment combined with a high-fat, high-sucrose, cholesterol-enriched (HFHSC) diet markedly amplified hepatic inflammation, characterized by the upregulation of pro-inflammatory genes and increased immune cell infiltration, including the expansion of lipid-associated macrophages (LAMs). Although circadian misalignment did not worsen glucose intolerance or hepatic steatosis, it altered hepatic metabolic gene expression, reflecting a broad reprogramming of immune and metabolic pathways. The circadian clock controls both FA profile and inflammatory process, and its misalignment aggravates MASLD by increasing liver inflammation. Targeting circadian regulators such as Rev-erbα in myeloid cells may offer a promising therapeutic avenue for controlling liver inflammation in MASLD.
• Med1 Deletion Reprograms Dental Epithelium into Primitive Hair-Forming Epidermal Architecture via Trp63 Driven Epigenetic Alterations
  GSE316847Mus musculus1 个样本2026-10-28

  Ectodermal fate decisions between tooth enamel and skin hair are governed by transcription factors, epigenetic mechanisms, and tissue architecture. Deletion of the Mediator subunit Med1, which links enhancer activity to transcriptional output, induces a striking lineage conversion characterized by ectopic hair formation in mouse incisors. Here, we define the cellular, transcriptional, and epigenetic mechanisms underlying this process. Single-cell and spatial transcriptomic analyses reveal extensive remodeling of the incisor epithelium following Med1 deletion, whereby dental pre-ameloblasts and SI cells convert into hair germ–like populations resembling ancestral hair-initiating cells while retaining dental identity. Epidermal fate is driven by the master regulator Trp63, enabling hair formation without follicles distinguishing this process from canonical skin hair regeneration. Mechanistically, epigenetic changes occur in which TRP63 co-localized with alternative MED12-containing enhancers to activate itself and downstream epidermal genes. Together, these findings suggest that Med1 loss promotes hair formation through unique reprogramming to an evolutionarily primitive epidermal state rather than direct trans-differentiation to skin epithelium, providing new insights in ectodermal plasticity.

  单细胞空间转录组
• Med1 Deletion Reprograms Dental Epithelium into Primitive Hair-Forming Epidermal Architecture via Trp63 Driven Epigenetic Mechanisms
  GSE316208Mus musculus12 个样本2026-10-28

  Ectodermal fate decisions between tooth enamel and skin hair are governed by transcription factors, epigenetic mechanisms, and tissue architecture. Deletion of the Mediator subunit Med1, which links enhancer activity to transcriptional output, induces a striking lineage conversion characterized by ectopic hair formation in mouse incisors. Here, we define the cellular, transcriptional, and epigenetic mechanisms underlying this process. Single-cell and spatial transcriptomic analyses reveal extensive remodeling of the incisor epithelium following Med1 deletion, whereby dental pre-ameloblasts and SI cells convert into hair germ–like populations resembling ancestral hair-initiating cells while retaining dental identity. Epidermal fate is driven by the master regulator Trp63, enabling hair formation without follicles distinguishing this process from canonical skin hair regeneration. Mechanistically, epigenetic changes occur in which TRP63 co-localized with alternative MED12-containing enhancers to activate itself and downstream epidermal genes. Together, these findings suggest that Med1 loss promotes hair formation through unique reprogramming to an evolutionarily primitive epidermal state rather than direct trans-differentiation to skin epithelium, providing new insights in ectodermal plasticity.

  单细胞空间转录组
• Soundwave Priming Enhances the Therapeutic Efficacy of Mesenchymal Stromal Cell–Derived Extracellular Vesicles in Acute Respiratory Distress Syndrome
  GSE316041Mus musculus8 个样本2026-10-28

  Our findings provide a robust model in which the UC-EVs cargo modulated by pFUS priming drives improved mitochondrial energetics, barrier protection, and resolution of inflammation, supporting the translational potential of pUC-EVs.
• Dual SGLT1 and 2 inhibition with sotagliflozin decreases oxidative stress in mice with hypertrophic cardiomyopathy due to tropomyosin E180G mutation
  GSE315790Mus musculus21 个样本2026-10-28

  Background. Hypertrophic cardiomyopathy (HCM) is associated with mitochondrial dysfunction and oxidative stress. Our goal was to determine the effects of the dual SGLT1 and SGLT2 inhibitor sotagliflozin (SOTA) on myocardial remodeling, diastolic function, mitochondrial gene expression and oxidative stress in mice with HCM due to the tropomyosin E180G mutation (E180G). Methods. Male E180G and non-carrier (NC) mice 7-8 weeks old were randomized to SOTA formulated in the chow (30 mg/kg chow) or control diet (CD) for 8 weeks. Cardiac structure and function were assessed by echocardiography at baseline, and after 4 and 8 weeks of treatment. At 8 weeks mice were sacrificed to assess myocardial histology, RNA expression, oxidative stress and oxidative sulfonylation of sarcoplasmic reticulum calcium ATPase (SERCA). Results. At baseline E180G mice had myocardial hypertrophy, interstitial fibrosis, diastolic dysfunction and atrial enlargement - all of which worsened over the next 8 weeks. In E180G mice treatment with SOTA for 8 weeks prevented further LV hypertrophy and atrial enlargement, decreased interstitial fibrosis and normalized diastolic function. Mitochondrial gene sets were downregulated, and oxidative stress was increased and associated with oxidative sulfonylation of SERCA at C674. SOTA treatment upregulated mitochondrial gene sets and prevented the increases in oxidative stress and SERCA oxidation. Upregulated fibrosis gene sets in E180G hearts were not affected by SOTA. Conclusion. In E180G HCM mice downregulation of mitochondrial gene sets is associated with increased oxidative stress and oxidative modification of SERCA. In E180G hearts, SOTA corrected the HCM phenotype, normalized diastolic function, upregulated mitochondrial gene sets, and decreased oxidative stress and SERCA oxidation. Upregulation of mitochondrial gene sets leading to improved mitochondrial function may improve energetics and decrease oxidative stress. Oxidative stress leads to oxidative modification of SERCA and stimulation of fibrosis pathways which may play a significant role in HCM, and thus provide an opportunity for therapeutic intervention with agents that improve mitochondrial function and/or decrease oxidative stress.
• Bulk RNA-seq atlas of cytokine-polarized murinebone-marrow-derived macrophages (BMDMs) across inflammatory, regulatory, and reparative stimuli
  GSE315641Mus musculus81 个样本2026-10-28

  Macrophages are highly plastic immune cells that adopt diverse functional states in response to local microenvironmental cues. In tissues, they contribute to host defense, maintain homeostasis, and coordinate responses to perturbations such as infection, injury, and inflammation. This functional diversity arises from their ability to integrate signals from cytokines, growth factors, and stromal interactions, particularly during tissue damage when macrophages transition from inflammatory to regulatory and reparative states. Despite increasing recognition of macrophage heterogeneity, most transcriptomic studies of macrophage polarization focus on a limited set of stimuli, providing an incomplete view of the cytokine-driven programs that shape macrophage behavior during inflammation and repair. Key mediators, including IL-4, IL-13, IL-33, IL-6, IL-10, GM-CSF, and TGF-β, induce distinct yet partially overlapping transcriptional responses that give rise to specialized and hybrid macrophage states. However, a systematic comparative analysis of these cytokine-induced programs remains lacking. To address this gap, we performed bulk RNA-sequencing of murine bone marrow–derived macrophages stimulated in vitro with a comprehensive panel of cytokines representing inflammatory, regulatory, and reparative pathways. This dataset enables direct comparison of cytokine-specific transcriptional programs, delineates classical, alternative, and hybrid activation states, and provides a resource for studying the molecular basis of macrophage plasticity.

  扰动筛选细胞图谱
• Electroconductive Patch Promotes Heart Repair by Directing Epicardial Cell Fate towards Endothelial Lineage
  GSE311450Mus musculus10 个样本2026-10-28

  By developing patches whose electroconductivity matches native myocardium (cardiac electroconductivity-matched patches, CemPs), we show that WT1⁺ EPDCs convert into functional endothelial cells within 14 days of MI, and increase infarct vascular density in adult mice.We employed genetic fate-mapping approaches in WT1CreERT2 H11ZsGtd mice to trace the origin of the newly generated endothelial cells, and combined with single-cell transcriptomics further identifies a previously uncharacterized transitional state cells which is voltage-sensitive and commits to the endothelial lineage via TRPC3–Ca²⁺ signaling.This work elucidates the relationship between the electrical conductivity of biomaterials and the endothelial differentiation potential of WT1⁺ EPDCs, clearly defining the cellular origin of electroconductive patch-induced angiogenesis in adult mammals post-MI.

  单细胞
• Mitochondrial ATP production promotes T cell differentiation and function by regulating chromatin accessibility [RNASeq3]
  GSE310052Mus musculus12 个样本2026-10-28

  Immune elimination of chronic infection or cancer requires cytotoxic CD8 T cells that adopt and maintain an effector phenotype. Cytotoxic T cell function is a bioenergetically demanding process and T cells subjected to chronic antigen exposure have compromised effector function despite high rates of glycolysis. Here we report the ability of the short chain fatty acid, D-α-hydroxybutyrate, to act as a signaling molecule that increases mitochondrial ATP production and drives the conversion of proliferating T cells into cytotoxic effector cells. DAHB signaling switches ATP production from glycolysis to fatty acid oxidation, even in glucose-replete media. This conversion suppresses both AMPK phosphorylation and the integrated stress response (ISR) in activated T cells while significantly elevating the level of the phosphagen, phosphocreatine (PCr). Both the PCr bioenergetic reserve and oxidative phosphorylation were required for T cell effector differentiation. DAHB-induction of CD8-effector gene transcription was coupled to bioenergetics by enhanced ATP-dependent remodeling of chromatin accessibility at effector gene loci. DAHB enhanced CD8 T cell antitumor activity both in vitro and in vivo, and DAHB treatment of transferred T cells led to persistent in vivo antitumor effects. Together, these findings link cellular bioenergetics to the regulation of chromatin accessibility and gene expression required to support effector function.
• 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.
• Alternative splicing plays an important role in fast chemical reprogramming [CUT&Tag]
  GSE292985Mus musculus12 个样本2026-10-28

  To investigate the role of Ptbp3 during reprogramming, CUT&Tag was carried out from the reprogramming intermediates transfected with shNC or shPtbp3.
• Muscles transcriptomic response to exercise
  GSE287162Mus musculus12 个样本2026-10-28

  The main goal of study was to see the transcriptional response to acute exercise in mice . For this the RNA seq was done in WT rest and WT exercise. We then want to reproduce the same result in HDAC3 ko mice and found the same result. Tissues were harvested immediately after the last session. RNA-seq identified that most differentially expressed genes (DEGs, exercise vs. rest) were upregulated upon exercise. We observed similar results in wild-type (WT) mice comparing exercise vs. rest and found that exercise-induced activation is independent of HDAC3, supporting the rationale for our investigation and demonstrate the robustness and reproducibility of the results that exercise-induced activation of our target gene is independent of HDAC3
• Lipid nanoparticle-mediated TFEB mRNA delivering for treatment of non-alcoholic fatty liver disease
  GSE283076Mus musculus16 个样本2026-10-28

  Non-alcoholic fatty liver disease (NAFLD) is a disease characterized by excessive lipid accumulation in the liver, often accompanied by obesity and insulin resistance. As the disease progresses, it can lead to non-alcoholic steatohepatitis (NASH), liver fibrosis, cirrhosis, and even hepatocellular carcinoma. The excessive activation of the mTORC1 complex promotes TFEB phosphorylation, thereby suppressing the TFEB-dependent lysosomal autophagy pathway and contributing to the development of NAFLD. Therefore, pharmacological activation of TFEB may offer a potential therapeutic strategy for NAFLD. However, currently, there is no drug that can directly activate TFEB. While mTORC1 inhibitors can indirectly activate TFEB, their use is limited by systemic side effects. In this study, we utilized lipid nanoparticles (LNP) to deliver TFEB mRNA to the liver. This targeted approach enhanced TFEB expression in hepatic cells, promoted autophagy, and mitigated NAFLD progression in a murine model.
• 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.
• Effect of YAP and KLF4 overexpression on gene expression of cerebral microvascular endothelial cells [RNA-Seq]
  GSE280201Mus musculus12 个样本2026-10-28

  Our preliminary findings revealed that YAP acts with KLF4. We here report overexpression of YAP and KLF4, either individually or in combination, led to significant changes in the transcriptomic profiles. YAP and KLF4 have substantial overlaps on co-regulation gene, which has a potential synergistic effect on gene expression. Our findings suggest that the co-regulated DEGs play pivotal roles in vascular and cellular processes, highlighting the synergistic effects of YAP and KLF4 on these biological activities.
• CCM2 knockout promotes transcriptional activity of YAP and KLF4 [CUT&Tag]
  GSE280200Mus musculus12 个样本2026-10-28

  CCM2 knockout dramatically increased the number of KLF4 regulatory genes, and similarly, the number of YAP regulatory genes surged. Consistently, the number of genes co-regulated by KLF4 and YAP also increased after CCM2 loss. Upon performing functional analyses of the genes co-regulated by KLF4 and YAP, we found that the genes in WT primary MBMECs were unable to enrich specific signaling pathways, while the genes in Ccm2-knockout primary MBMECs were enriched in several pathways, including SMAD binding, Rho GTPase binding, kinase regulator activity, et al
• 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.
• Transcriptomic analysis of mucosal immunity in mouse lung tissues induced by sequential Sad23L-RSV vaccination
  GSE352070Mus musculus15 个样本2026-10-27

  We performed transcriptomic analysis of lung tissues from BALB/c mice vaccinated with a novel adenovirus-vectored RSV vaccine (Sad23L-RSV) via an intranasal prime/intramuscular boost regimen. Lung tissues were collected at days 0, 2, 7, and 28 after the booster immunization to investigate the molecular mechanisms of durable mucosal immunity.
• 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.