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1. ⭐ GSE293427 糖尿病血管内皮细胞-巨噬细胞相互作用图谱：TREM2 在血管炎症和缺血反应中的作用 [空间转录组学]

• ✍️ 作者：未知作者
• 🏷️ 关键词：macrophage、inflammation、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Naseeb Malhi ; Viola Luo ; Xiaofang Tang ; Zhen ChenSeries Type : OtherOrganism : Homo sapiensDiabetes mellitus (DM) significantly accelerates vascular diseases like peripheral arterial disease (PAD). Endothelial cells (ECs) and macrophages (MΦs) singularly and synergistically are important contributors to DM-associated vascular dysfunction. Single-cell (sc) profiling technologies are revealing the true heterogeneity of ECs and MΦs, but how this cellular diversity translates to cell-cell interactions, and consequentially vascular function, remains unknown. We leveraged scRNA sequencing and spatial transcriptome (ST) profiling to analyze human mesenteric arteries from non-diabetic (ND) and type 2 diabetic (T2D) donors. We generated a transcriptome and interactome map encompassing the major arterial cells and highlighted Triggering Receptor Expressed on Myeloid Cells 2 (TREM2) as a top T2D-induced gene in mononuclear phagocytes (MPs), with concomitant increases of TREM2 ligands in ECs. We verified DM-associated TREM2 induction in cell and mouse models, and found that TREM2 inhibition decreases pro-inflammatory responses in MPs and ECs, as well as increases EC migration in vitro. Furthermore, TREM2 inhibition using a neutralizing antibody enhanced ischemic recovery and flow reperfusion in DM mice subjected to hindlimb ischemia, suggesting that TREM2 promotes ischemic injury in DM. Finally, in human PAD, co-existing DM was associated with greater expression of TREM2 and its interaction with ECs, with a further increase in ischemic tissue compared to patient-matched non-ischemic tissue. Collectively, our study presents the first atlas of human diabetic vessels with single cell and spatial resolution, and identifies TREM2-EC interaction as a key driver of diabetic vasculopathies, the targeting of which may offer an opportunity to ameliorate vascular dysfunction associated with DM-PAD.
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2. ⭐ GSE300265 单细胞转录组学揭示了老年人对 COVID-19 mRNA 疫苗无应答者中 B 细胞反应改变和 T 细胞衰老的特征

• ✍️ 作者：未知作者
• 🏷️ 关键词：T cell、B cell、single-cell、transcriptomics
• 📝 描述：Contributors : Jeeda Ismail ; Banumathi Tamilselvan ; Michael Rubsamen ; Jilian Petrosky ; Brian Richardson ; Leah Zagore ; Oladayo A Oyebanji ; Debbie Keresztesy ; Michael Payne ; Dennis Wilk ; Lenore Carias ; Htin Aung ; Kerri St. Denis ; Maeghanm Sheehan ; Brigid M Wilson ; Alejandro B Balazs ; Stefan Gravenstein ; Christopher L King ; David H Canaday ; Cheryl M Cameron ; Mark J CameronSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThe immune response to COVID-19 vaccines is diminished in older individuals. To understand the underlying immunobiology, we analyzed single-cell RNA-seq data from PBMCs of SARS-CoV-2 naïve nursing home residents with varying humoral responses following BNT162b2 vaccination and validated via flow cytometry. Responders (>4500 AU/mL anti-spike titers) showed enrichment for naïve B cell (IGHD, BACH2, CD22) and naïve CD4 T cell and early Tfh-related genes (CCR7, TCF7, LEF1, IL6ST, TGFBR2). Non-responders (<20 AU/mL) displayed elevated markers of T cell senescence (KLRG1, CCL4, CCL5, IL32), immune exhaustion (PD-1), and inflammation (TNF-α, IFN-γ). Flow cytometry revealed reduced CD4 T and B cell frequencies but higher CD8 T and NK cells in non-responders. Despite reduced B cell frequency, non-responders upregulated plasma B cell genes (PRDM1, XPB1, IRF4), suggesting dysregulated B cell differentiation. Our findings point to impaired lymphocyte responses and increased immunosenescence in non-responders, emphasizing the need for enhanced vaccine strategies in aging populations.
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3. ⭐ GSE317209 绘制糖尿病血管内皮细胞-巨噬细胞相互作用图谱：TREM2 在血管炎症和缺血反应中的作用 [bulk RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：macrophage、inflammation、RNA-seq
• 📝 描述：Contributors : Naseeb K Malhi ; Dongqiang Yuan ; Yingjun Luo ; Zhen B ChenSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensDiabetes mellitus (DM) significantly accelerates vascular diseases like peripheral arterial disease (PAD). Endothelial cells (ECs) and macrophages (MΦs) singularly and synergistically are important contributors to DM-associated vascular dysfunction. Single-cell (sc) profiling technologies are revealing the true heterogeneity of ECs and MΦs, but how this cellular diversity translates to cell-cell interactions, and consequentially vascular function, remains unknown. We leveraged scRNA sequencing and spatial transcriptome (ST) profiling to analyze human mesenteric arteries from non-diabetic (ND) and type 2 diabetic (T2D) donors. We generated a transcriptome and interactome map encompassing the major arterial cells and highlighted Triggering Receptor Expressed on Myeloid Cells 2 (TREM2) as a top T2D-induced gene in mononuclear phagocytes (MPs), with concomitant increases of TREM2 ligands in ECs. We verified DM-associated TREM2 induction in cell and mouse models, and found that TREM2 inhibition decreases pro-inflammatory responses in MPs and ECs, as well as increases EC migration in vitro. Furthermore, TREM2 inhibition using a neutralizing antibody enhanced ischemic recovery and flow reperfusion in DM mice subjected to hindlimb ischemia, suggesting that TREM2 promotes ischemic injury in DM. Finally, in human PAD, co-existing DM was associated with greater expression of TREM2 and its interaction with ECs, with a further increase in ischemic tissue compared to patient-matched non-ischemic tissue. Collectively, our study presents the first atlas of human diabetic vessels with single cell and spatial resolution, and identifies TREM2-EC interaction as a key driver of diabetic vasculopathies, the targeting of which may offer an opportunity to ameliorate vascular dysfunction associated with DM-PAD.
• 🔗 查看原文

4. ⭐ GSE293428 绘制糖尿病血管内皮细胞-巨噬细胞相互作用图谱：TREM2 在血管炎症和缺血反应中的作用 [scRNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：macrophage、inflammation、scRNA
• 📝 描述：Contributors : Naseeb Malhi ; Viola Luo ; Xiaofang Tang ; Zhen ChenSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensDiabetes mellitus (DM) significantly accelerates vascular diseases like peripheral arterial disease (PAD). Endothelial cells (ECs) and macrophages (MΦs) singularly and synergistically are important contributors to DM-associated vascular dysfunction. Single-cell (sc) profiling technologies are revealing the true heterogeneity of ECs and MΦs, but how this cellular diversity translates to cell-cell interactions, and consequentially vascular function, remains unknown. We leveraged scRNA sequencing and spatial transcriptome (ST) profiling to analyze human mesenteric arteries from non-diabetic (ND) and type 2 diabetic (T2D) donors. We generated a transcriptome and interactome map encompassing the major arterial cells and highlighted Triggering Receptor Expressed on Myeloid Cells 2 (TREM2) as a top T2D-induced gene in mononuclear phagocytes (MPs), with concomitant increases of TREM2 ligands in ECs. We verified DM-associated TREM2 induction in cell and mouse models, and found that TREM2 inhibition decreases pro-inflammatory responses in MPs and ECs, as well as increases EC migration in vitro. Furthermore, TREM2 inhibition using a neutralizing antibody enhanced ischemic recovery and flow reperfusion in DM mice subjected to hindlimb ischemia, suggesting that TREM2 promotes ischemic injury in DM. Finally, in human PAD, co-existing DM was associated with greater expression of TREM2 and its interaction with ECs, with a further increase in ischemic tissue compared to patient-matched non-ischemic tissue. Collectively, our study presents the first atlas of human diabetic vessels with single cell and spatial resolution, and identifies TREM2-EC interaction as a key driver of diabetic vasculopathies, the targeting of which may offer an opportunity to ameliorate vascular dysfunction associated with DM-PAD.
• 🔗 查看原文

5. ⭐ GSE230327 BRD8 是克服 HR+/HER2+ 乳腺癌对 ER/HER2 双重阻断疗法耐药性的治疗靶点 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、resistance、scRNA
• 📝 描述：Contributors : Ang Gao ; Parth Khatri ; Huy Q Dinh ; Wei XuSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensHormone receptor (HR)-positive, HER2-positive breast cancers are resistant to endocrine and anti-HER2 therapies due to crosstalk between estrogen receptor (ER) and HER2. However, how anti-HER2 agents activate ER as a mechanism of resistance remains unknown. Using single-cell RNA sequencing, we identified Bromodomain Containing Protein 8 (BRD8) as a major mediator of ER activation in response to neratinib, a HER2 tyrosine kinase inhibitor. BRD8 expression was rapidly induced by various anti-HER2 agents (neratinib, lapatinib and trastuzumab) and its expression positively correlates with ER. BRD8 regulates both ER-dependent and -independent growth promoting pathways. Moreover, BRD8 ablation re-sensitizes fulvestrant- or neratinib-resistant HR+/HER2+ cells to neratinib, suggesting that combinatorial targeting of BRD8 and HER2 attenuates signal crosstalk and possibly overcomes treatment resistance to dual anti-ER/HER2 blockade therapy. This work identifies BRD8 as not only a central hub for ER signaling activation upon anti-HER2 treatment, but also a druggable vulnerability for treating HR+/HER2+ breast cancer.
• 🔗 查看原文

6. GSE230326 BRD8 是克服 HR+/HER2+ 乳腺癌对 ER/HER2 双重阻断疗法耐药性的治疗靶点 [bulkRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、resistance
• 📝 描述：Contributors : Ang Gao ; Parth Khatri ; Huy Q Dinh ; Wei XuSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensHormone receptor (HR)-positive, HER2-positive breast cancers are resistant to endocrine and anti-HER2 therapies due to crosstalk between estrogen receptor (ER) and HER2. However, how anti-HER2 agents activate ER as a mechanism of resistance remains unknown. Using single-cell RNA sequencing, we identified Bromodomain Containing Protein 8 (BRD8) as a major mediator of ER activation in response to neratinib, a HER2 tyrosine kinase inhibitor. BRD8 expression was rapidly induced by various anti-HER2 agents (neratinib, lapatinib and trastuzumab) and its expression positively correlates with ER. BRD8 regulates both ER-dependent and -independent growth promoting pathways. Moreover, BRD8 ablation re-sensitizes fulvestrant- or neratinib-resistant HR+/HER2+ cells to neratinib, suggesting that combinatorial targeting of BRD8 and HER2 attenuates signal crosstalk and possibly overcomes treatment resistance to dual anti-ER/HER2 blockade therapy. This work identifies BRD8 as not only a central hub for ER signaling activation upon anti-HER2 treatment, but also a druggable vulnerability for treating HR+/HER2+ breast cancer.
• 🔗 查看原文

7. GSE306262 星形胶质细胞糖皮质激素受体信号传导限制神经元可塑性 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：Neuronal、RNA-seq
• 📝 描述：Contributors : Bruno Gegenhuber ; Takuma Sonoda ; Lisa Traunmüller ; Christopher P Davis ; Shon A Koren ; Eric C Griffith ; Chinfei Chen ; Michael E GreenbergSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusSensory experience refines neural circuits during critical periods of postnatal development. Although neuronal activity is known to orchestrate the circuit wiring that underlies this process, the environmental cues that restrain developmental plasticity as animals mature are less clear. Here, we examine the experience-dependent maturation of the mouse primary visual cortex (V1) across postnatal development using paired single-cell transcriptomic and chromatin accessibility sequencing. In addition to identifying the activity-dependent gene programs that emerge within each cortical cell type, we find that light exposure drives astrocyte maturation through cell type-specific recruitment of the glucocorticoid receptor (Nr3c1/GR) to chromatin. Astrocyte GR signaling activates an extensive gene regulatory program that is partially conserved in human brain development and promotes maturation processes that may trigger critical period closure. Collectively, these findings reveal that astrocyte GR signaling restricts neuronal plasticity. ​​Glucocorticoid regulation of astrocyte maturation may also contribute to the effects of early-life stress across the brain, and the disruption of this process may increase susceptibility to neuropsychiatric disease.
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8. GSE299347 星形胶质细胞糖皮质激素受体信号传导限制神经元可塑性 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：Neuronal、ATAC-seq
• 📝 描述：Contributors : Bruno Gegenhuber ; Takuma Sonoda ; Lisa Traunmüller ; Christopher P Davis ; Shon A Koren ; Eric C Griffith ; Chinfei Chen ; Michael E GreenbergSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusSensory experience refines neural circuits during critical periods of postnatal development. Although neuronal activity is known to orchestrate the circuit wiring that underlies this process, the environmental cues that restrain developmental plasticity as animals mature are less clear. Here, we examine the experience-dependent maturation of the mouse primary visual cortex (V1) across postnatal development using paired single-cell transcriptomic and chromatin accessibility sequencing. In addition to identifying the activity-dependent gene programs that emerge within each cortical cell type, we find that light exposure drives astrocyte maturation through cell type-specific recruitment of the glucocorticoid receptor (Nr3c1/GR) to chromatin. Astrocyte GR signaling activates an extensive gene regulatory program that is partially conserved in human brain development and promotes maturation processes that may trigger critical period closure. Collectively, these findings reveal that astrocyte GR signaling restricts neuronal plasticity. ​​Glucocorticoid regulation of astrocyte maturation may also contribute to the effects of early-life stress across the brain, and the disruption of this process may increase susceptibility to neuropsychiatric disease.
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9. GSE324961 微RNA-132 可减轻阿尔茨海默病患者诱导多能干细胞衍生的小胶质细胞的炎症

• ✍️ 作者：未知作者
• 🏷️ 关键词：inflammation、Alzheimer
• 📝 描述：Contributors : Amber Penning ; Sarah Snoeck ; Olmo Ruiz Ormaechea ; Dilara Ayyildiz ; Oliver Polzer ; Martin Buitrago-Arango ; Raffaella Copabianco ; Fred de Winter ; Sriram Balusu ; Joost Verhaagen ; Carlos P. Fitzsimons ; Constantin d’Ydewalle ; Paul J. Lucassen ; Dieder Moechars ; Lujia Zhou ; Salta EvgeniaSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensMicroglia, the resident immune cells of the brain, are increasingly recognized as key contributors to Alzheimer’s disease (AD) pathology. Multiple studies have identified microRNA-132 (miR-132) as one of the most significantly downregulated microRNAs in AD. Apart from well-established pleiotropic regulatory functions in neurons, previous evidence also suggested a role for miR-132 in regulating (neuro)inflammation. Yet, the precise mechanisms by which miR-132 impacts microglia remain unknown. In this study, we investigated the role of miR-132 in modulating microglial gene expression and function using gain- and loss-of-function approaches in human-induced pluripotent stem cell (iPSC)-derived microglia (iMGs) from both healthy controls and sporadic AD (sAD) patients. Our findings indicate that while miR-132 may not be indispensable for some baseline microglial functions, increasing its expression in sAD iMGs can reverse disease-associated gene expression changes and attenuate inflammatory responses. To further explore its therapeutic potential, we overexpressed miR-132 in hippocampal neurons of an AD mouse model, employing a clinically relevant adeno-associated viral (AAV) delivery method. miR-132 overexpression was well-tolerated and induced non-cell autonomous effects in microglia. This study sheds light into the regulatory role of miR-132 in microglia under both physiological and AD conditions, and emphasizes the importance of optimizing safe dosage parameters for future clinical applications.
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10. GSE319686 CTNNB1 和 PTEN 的共突变协同促进子宫内膜癌的 EMT 并驱动肿瘤的侵袭性进展。

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer
• 📝 描述：Contributors : TaeHoon Kim ; JaeWook JeongSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusEndometrioid endometrial cancer (EEC) is the most common gynecologic malignancy, with poor outcomes in advanced stages. Co-mutations in PTEN and CTNNB1 are frequent and linked to poor prognosis, but their functional roles remain unclear. Using uterine-specific Pten knockout and stabilized β-catenin mutant mice (Pgrcre/+Ptenf/fCtnnb1f(ex3)/+; Ptend/dCtnnb1f(ex3)/+), we found markedly reduced survival, early-onset invasive adenocarcinoma, and aggressive metastatic disease compared to Pgrcre/+Ptenf/f; Ptend/d mice. Transcriptomic and histopathological analyses revealed activation of oncogenic pathways (WNT/β-catenin, PI3K/AKT, Hedgehog, EMT), with loss of E-cadherin and upregulation of SNAIL confirming EMT. These findings show that PTEN–CTNNB1 co-mutations synergistically drive EMT and tumor progression, defining a distinct aggressive subtype of EEC.
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1. ⭐ 科学家将益生菌转化为肿瘤猎杀者，对抗癌症

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、bacteria、regex:bacter(ia|ial|ium)
• 📝 描述：Scientists have engineered probiotic bacteria to act as tumor-seeking drug factories. In mice, these bacteria infiltrated tumors and produced a cancer-fighting drug right where it was needed. This targeted approach could make treatments more effective and reduce side effects. More research is needed before it can be tested in people.
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2. 这种病毒疗法能显著增强免疫系统对抗脑癌的能力。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune
• 📝 描述：Scientists have found a way to make one of the most aggressive brain tumors vulnerable to the immune system. A single injection of a modified virus can invade glioblastoma, kill cancer cells, and summon immune fighters deep into the tumor. These immune cells persist and attack, which was linked to longer survival in patients.
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3. 一项新研究表明，这种常用疫苗可将心脏病风险降低近一半。

• ✍️ 作者：未知作者
• 🏷️ 关键词：vaccine
• 📝 描述：A shingles vaccine might double as a powerful heart protector. In people already at high risk, it cut major cardiac events by 46% and deaths by an impressive 66% within a year. Scientists think preventing shingles may also stop clot-related complications that can lead to heart attacks and strokes. The effect is so strong, it rivals the benefits of quitting smoking.
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• GSE312765 野生型和 Uhrf1-/- ESC 的全基因组亚硫酸氢盐测序 (WGBS)
• GSE293557 靶向癌症干细胞和癌细胞的纳米疫苗可减少术后肿瘤复发 [meRIP-seq]
• GSE293556 靶向癌症干细胞和癌细胞的纳米疫苗可减少术后肿瘤复发 [RIP-Seq]
• GSE320054 利用 CaMPARI-seq 进行分子和功能解析揭示了分离光流依赖性行为的神经元组织
• GSE305142 L型电压门控Ca2+通道通过非经典Hedgehog信号通路控制T细胞杀伤
• GSE300853 集体非结构化相互作用驱动转录因子与染色质的结合。[ChIP-Seq]
• GSE316698 对来自 49 名墨西哥参与者的人类皮下脂肪组织活检样本进行单核 RNA 测序
• GSE306582 星形胶质细胞糖皮质激素受体信号传导限制神经元可塑性 [SHARE-seq]
• GSE306265 星形胶质细胞糖皮质激素受体信号传导限制神经元可塑性
• GSE306263 星形胶质细胞糖皮质激素受体信号传导限制神经元可塑性 [snRNA-seq]
• GSE306261 星形胶质细胞糖皮质激素受体信号传导限制神经元可塑性 [CUT&RUN]
• GSE304204 HnRNP C binding to inverted Alu elements protects the transcriptome from pre-mRNA circularization
• GSE300628 HER2阳性乳腺癌
• GSE289592 人诱导多能干细胞来源的肝星状细胞在肝脏类器官中的作用：促进成熟并在血管化中发挥重要作用 [scRNA-Seq]
• GSE325023 拟南芥 PsbS 和 β-碳酸酐酶过表达株系对碳酸氢盐施肥的转录组分析
• GSE324916 DEK 中丝氨酸 287/288 的磷酸化调节细胞类型特异性染色质占据和压缩 [ChIP-Seq]
• GSE322686 小鼠模型中狼疮性肾炎进展的纵向多组学和空间转录组学分析
• GSE289650 阻断胰岛素信号与 PI3K 抑制剂协同抑制 MYCN 儿童高级别胶质瘤生长 [RNA-seq2]
• GSE289649 阻断胰岛素信号传导与 PI3K 抑制剂协同抑制 MYCN 儿童高级别胶质瘤生长 [RNA-seq1]
• GSE276138 ac4C 乙酰转移酶 Nat10 促进 RNA 稳定性以支持造血干细胞命运 [RNA-seq-mouse]
• GSE276137 ac4C 乙酰转移酶 Nat10 促进 RNA 稳定性以支持造血干细胞命运 [RNA-seq-32D]