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MicroRNA-502-3p regulates GABAergic synapse function in hippocampal neurons

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Neural Regeneration Research 2024年第12期19卷 2698-2707页

作者： Bhupender Sharma Melissa MTorres Sheryl Rodriguez Laxman Gangwani Subodh Kumar Center of Emphasis in Neuroscience Department of Molecular and Translational MedicinePaul L.Foster School of MedicineTexas Tech University Health Sciences CenterEl PasoTXUSA Bond Life sciences Center and Department of Veterinary Pathobiology University of MissouriColumbiaMOUSA L.Frederick Francis graduate school of biomedical sciences Texas Tech University Health Sciences CenterEl PasoTXUSA

Gamma-aminobutyric acid(GABA)ergic neurons,the most abundant inhibitory neurons in the human brain,have been found to be reduced in many neurological disorders,including Alzheimer's disease and Alzheimer's disease-related dementia.Our previous study identified the upregulation of microRNA-502-3p(miR-502-3p)and downregulation of GABA type A receptor subunitα-1 in Alzheimer's disease synapses.This study investigated a new molecular relationship between miR-502-3p and GABAergic synapse function.In vitro studies were perfo rmed using the mouse hippocampal neuronal cell line HT22 and miR-502-3p agomiRs and antagomiRs.In silico analysis identified multiple binding sites of miR-502-3p at GABA type A receptor subunitα-1 mRNA.Luciferase assay confirmed that miR-502-3p targets the GABA type A receptor subunitα-1 gene and suppresses the luciferase activity.Furthermore,quantitative reve rse transcription-polymerase chain reaction,miRNA in situ hybridization,immunoblotting,and immunostaining analysis confirmed that overexpression of miR-502-3p reduced the GABA type A receptor subunitα-1 level,while suppression of miR-502-3p increased the level of GABA type A receptor subunitα-1 protein.Notably,as a result of the overexpression of miR-502-3p,cell viability was found to be reduced,and the population of necrotic cells was found to be increased.The whole cell patch-clamp analysis of human-GABA receptor A-α1/β3/γ2L human embryonic kidney(HEK)recombinant cell line also showed that overexpression of miR-502-3p reduced the GABA current and overall GABA function,suggesting a negative correlation between miR-502-3p levels and GABAergic synapse function.Additionally,the levels of proteins associated with Alzheimer s disease were high with miR-502-3p overexpression and reduced with miR-502-3p suppression.The present study provides insight into the molecular mechanism of regulation of GABAergic synapses by miR-502-3p.We propose that micro-RNA,in particular miR-502-3p,could be a potential therapeutic to rget to modulate GABAergic synapse f

关键词： Alzheimer's disease GABAergic synapse gamma-aminobutyric acid type A receptor subunitα-1(GABRα1) microRNA-502-3p(miR-502-3p) miRNA in situ hybridization Patch-clamp

Integrative genomic and transcriptomic profiling of pulmonary sarcomatoid carcinoma identifies molecular subtypes associated with distinct immune features and clinical outcomes

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Cancer Innovation 2024年第3期3卷 81-94页

作者： Sahil Seth Runzhe Chen Yang Liu Junya Fujimoto Lingzhi Hong Alexandre Reuben Susan Varghese Carmen Behrens Tina McDowell Luisa Solis Soto Cara Haymaker Annikka Weissferdt Neda Kalhor Jia Wu Xiuning Le Natalie I Vokes Chao Cheng John V.Heymach Don L.Gibbons P.Andrew Futreal Ignacio IWistuba Humam Kadara Jianhua Zhang Cesar Moran Jianjun Zhang Department of Genomic Medicine The University of Texas MD Anderson Cancer CenterHoustonTexasUSA TRACTION The University of Texas MD Anderson Cancer CenterHoustonTexasUSA graduate school of biomedical sciences The University of Texas MD Anderson and the University of Texas Health Science CenterHoustonTexasUSA Department of Thoracic/Head and Neck Medical Oncology The University of Texas MD Anderson Cancer CenterHoustonTexasUSA Department of Translational Molecular Pathology The University of Texas MD Anderson Cancer CenterHoustonTexasUSA Department of Epidemiology The University of Texas MD Anderson Cancer CenterHoustonTexasUSA Department of Pathology The University of Texas MD Anderson Cancer CenterHoustonTexasUSA Department of Imaging Physics The University of Texas MD Anderson Cancer CenterHoustonTexasUSA Department of Medicine Baylor College of MedicineHoustonTexasUSA

Background:Pulmonary sarcomatoid carcinoma(PSC)is a rare and aggressive subtype of non-small cell lung cancer(NSCLC),characterized by the presence of epithelial and sarcoma-like components.The molecular and immune landscape of PSC has not been well defined.Methods:Multiomics profiling of 21 pairs of PSCs with matched normal lung tissues was performed through targeted high-depth DNA panel,whole-exome,and RNA sequencing.We describe molecular and immune features that define subgroups of PSC with disparate genomic and immunogenic features as well as distinct clinical outcomes.Results:In total,27 canonical cancer gene mutations were identified,with TP53 the most frequently mutated gene,followed by KRAS.Interestingly,most TP53 and KRAS mutations were earlier genomic events mapped to the trunks of the tumors,suggesting branching evolution in most PSC tumors.We identified two distinct molecular subtypes of PSC,driven primarily by immune infiltration and signaling.The Immune High(IM-H)subtype was associated with superior survival,highlighting the impact of immune infiltration on the biological and clinical features of localized PSCs.Conclusions:We provided detailed insight into the mutational landscape of PSC and identified two molecular subtypes associated with prognosis.IM-H tumors were associated with favorable recurrence-free survival and overall survival,highlighting the importance of tumor immune infiltration in the biological and clinical features of PSCs.

关键词： genomic immune pulmonary sarcomatoid carcinoma survival

Author Correction:Enhanced CD19 activity in B cells contributes to immunodeficiency in mice deficient in the ICF syndrome gene Zbtb24

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Cellular & Molecular Immunology 2024年第1期21卷 100-100页

作者： Zhengzhou Ying Swanand Hardikar Joshua B.Plummer Tewfik Hamidi Bin Liu Yueping Chen Jianjun Shen Yunxiang Mu Kevin M.McBride Taiping Chen Department of Epigenetics and Molecular Carcinogenesis The University of Texas MD Anderson Cancer Center Houston TX 77030 USA Program in Genetics and Epigenetics The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences Houston TX 77030 USA

In the sentence beginning‘To trace cell proliferation,FO and MZ B cells’and the sentence beginning‘For cell activation,naïve B cells or CH12F3 cells’in this article,the[10 ng/ml]‘F(ab’)_(2)fragment goat anti-mouse IgM’should have read‘10μg/ml F(ab’)_(2)fragment goat anti-mouse IgM’.The original article has been corrected.

关键词： immunodeficiency CD19 deficient

NetBCE: An Interpretable Deep Neural Network for Accurate Prediction of Linear B-cell Epitopes

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Genomics, Proteomics & Bioinformatics 2022年第5期20卷 1002-1012页

作者： Haodong Xu Zhongming Zhao Center for Precision Health School of Biomedical InformaticsThe University of Texas Health Science Center at HoustonHoustonTX 77030USA Human Genetics Center School of Public HealthThe University of Texas Health Science Center at HoustonHoustonTX 77030USA The university of texas MD Anderson Cancer Center UTHealth houston graduate school of biomedical sciences HoustonTX 77030USA Department of biomedical Informatics Vanderbilt University Medical CenterNashvilleTN 37203USA

Identification of B-cell epitopes(BCEs)plays an essential role in the development of peptide vaccines and immuno-diagnostic reagents,as well as antibody design and production.In this work,we generated a large benchmark dataset comprising 124,879 experimentally supported linear epitope-containing regions in 3567 protein clusters from over 1.3 million B cell assays.Analysis of this curated dataset showed large pathogen diversity covering 176 different families.The accuracy in linear BCE prediction was found to strongly vary with different features,while all sequencederived and structural features were informative.To search more efficient and interpretive feature representations,a ten-layer deep learning framework for linear BCE prediction,namely Net BCE,was *** BCE achieved high accuracy and robust performance with the average area under the curve(AUC)value of 0.8455 in five-fold cross-validation through automatically learning the informative classification *** BCE substantially outperformed the conventional machine learning algorithms and other tools,with more than 22.06%improvement of AUC value compared to other tools using an independent dataset.Through investigating the output of important network modules in Net BCE,epitopes and non-epitopes tended to be presented in distinct regions with efficient feature representation along the network layer hierarchy.The Net BCE is freely available at https://***/bsml320/Net BCE.

关键词： prediction network value

Ferroptosis as an important driver of lupus

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Protein & Cell 2022年第5期13卷 313-315页

作者： Chao Mao Guang Lei Li Zhuang Boyi Gan Department of Experimental Radiation Oncology The University of Texas MD Anderson Cancer CenterHoustonTXUSA The university of texas MD Anderson UTHealth graduate school of biomedical sciences HoustonTXUSA

Systemic lupus erythematosus(SLE),the most common form of lupus,is a chronic autoimmune disorder characterized by a global loss of self-tolerance and hyper-activation of both innate and adaptive immune systems(Kaul et al.,2016).Neutrophils,the most abundant leukocytes in human blood,have a critical role in maintaining immune surveillance and tissue homeostasis,and its dysregulation is of high relevance to SLE(Ricklin et al.,2010).In patients with SLE,accelerated neutrophil death and the deficiency in clearing dying neutrophils cause nuclear and cytoplasmic antigen exposure,excessive production of type I interferon(IFN),and neutrophil extracellular trap(NET)release,subsequently inducing autoimmune responses(Garcia-Romo et al.,2011).Dysregulated neutrophil death is believed to be a major cause of SLE;however,the underlying mechanism of neutrophil death in SLE is not well-defined.

关键词： al. lupus autoimmune

Enhanced CD19 activity in B cells contributes to immunodeficiency in mice deficient in the ICF syndrome gene Zbtb24

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Cellular & Molecular Immunology 2023年第12期20卷 1487-1498页

作者： Zhengzhou Ying Swanand Hardikar Joshua B.Plummer Tewfik Hamidi Bin Liu Yueping Chen Jianjun Shen Yunxiang Mu Kevin M.McBride Taiping Chen Department of Epigenetics and Molecular Carcinogenesis The University of Texas MD Anderson Cancer CenterHoustonTX77030USA Program in Genetics and Epigenetics The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical SciencesHoustonTX77030USA

Immunodeficiency,centromeric instability,and facial anomalies(ICF)syndrome is a rare autosomal recessive disorder characterized by DNA hypomethylation and antibody deficiency.It is caused by mutations in DNMT3B,ZBTB24,CDCA7,or HELLS.While progress has been made in elucidating the roles of these genes in regulating DNA methylation,little is known about the pathogenesis of the life-threatening hypogammaglobulinemia phenotype.Here,we show that mice deficient in Zbtb24 in the hematopoietic lineage recapitulate the major clinical features of patients with ICF syndrome.Specifically,Vav-Cre-mediated ablation of Zbtb24 does not affect lymphocyte development but results in reduced plasma cells and low levels of IgM,IgG1,and IgA.Zbtb24-deficient mice are hyper and hypo-responsive to T-dependent and T-independent type 2 antigens,respectively,and marginal zone B-cell activation is impaired.Mechanistically,Zbtb24-deficient B cells show severe loss of DNA methylation in the promoter region of Il5ra(interleukin-5 receptor subunit alpha),and Il5ra derepression leads to elevated CD19 phosphorylation.Heterozygous disruption of Cd19 can revert the hypogammaglobulinemia phenotype of Zbtb24-deficient mice.Our results suggest the potential role of enhanced CD19 activity in immunodeficiency in ICF syndrome.

关键词： ICF syndrome ZBTB24 CD19 IL-5Ra hypogammaglobulinemia

Uncovering the IL-1β-PCAF-NNT axis:A new player in ferroptosis and tumor immune evasion

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Cancer Communications 2023年第9期43卷 1048-1050页

作者： Qidong Li Boyi Gan Department of Experimental Radiation Oncology The University of Texas MD Anderson Cancer CenterHoustonTXUSA The university of texas MD Anderson UTHealth graduate school of biomedical sciences HoustonTXUSA

Chronic inflammation is recognized as a crucial hallmark of cancer.Interleukin-1β(IL-1β),one of the proinflammatory cytokines,plays an ambiguous or even contradictory role in cancer development[1].While increased expression of IL-1βin the tumor microenvironment is associated with tumor development,and invasiveness[1],it has also shown anti-tumorigenic effects in other contexts[2].Therefore,it is difficult to define IL-1β’s role as either tumor-promoting or anti-tumorigenic in cancers.Further investigation of IL-1βin specific contexts is essential to comprehensively understand its role in cancers.

关键词： tumor inflammation Interleukin

PKCβII-ACSL4 pathway mediating ferroptosis execution and anti-tumor immunity

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Cancer Communications 2022年第7期42卷 583-586页

作者： Guang Lei Amber Horbath Zhuang Li Boyi Gan Department of Experimental Radiation Oncology The University of Texas MD Anderson Cancer CenterHoustonTX 77030USA The university of texasMD Anderson UTHealth graduate school of biomedical sciences HoustonTX 77030USA

Ferroptosis is an iron-dependent form of regulated cell death that results from oxidative damages of membrane phospholipids,and is mechanistically and morphologically unique compared to other cell death modalities,such as apoptosis and necroptosis[1].Excessive ferroptosis is indicative of many pathological conditions,including cardiovascular diseases,neurodegenerative diseases,and acute organ injury,whereas ferroptosis impairment has been shown to fuel tumor progression and metastasis;therefore,targeting ferroptosis represents a promising strategy for treating these diseases[2-10].Ferroptosis is triggered by a lethal accumulation of lipid peroxides on the cell membrane.

关键词： immunity diseases death

deCS:A Tool for Systematic Cell Type Annotations of Single-cell RNA Sequencing Data among Human Tissues

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Genomics, Proteomics & Bioinformatics 2023年第2期21卷 370-384页

作者： Guangsheng Pei Fangfang Yan Lukas M.Simon Yulin Dai Peilin Jia Zhongming Zhao Center for Precision Health School of Biomedical InformaticsThe University of Texas Health Science Center at HoustonHoustonTX 77030USA Therapeutic Innovation Center Baylor College of MedicineHoustonTX 77030USA Human Genetics Center School of Public HealthThe University of Texas Health Science Center at HoustonHoustonTX 77030USA MD Anderson Cancer Center UTHealth graduate school of biomedical sciences HoustonTX 77030USA Department of biomedical Informatics Vanderbilt University Medical CenterNashvilleTN 37203USA CAS Key Laboratory of Genomic and Precision Medicine Beijing Institute of GenomicsChinese Academy of Sciences and China National Center for BioinformationBeijing 100101China

Single-cell RNA sequencing(scRNA-seq)is revolutionizing the study of complex and dynamic cellular mechanisms.However,cell type annotation remains a main challenge as it largely relies on a priori knowledge and manual curation,which is cumbersome and subjective.The increasing number of scRNA-seq datasets,as well as numerous published genetic studies,has motivated us to build a comprehensive human cell type reference atlas.Here,we present decoding Cell type Specificity(deCS),an automatic cell type annotation method augmented by a comprehensive collection of human cell type expression profiles and marker genes.We used deCS to annotate scRNAseq data from various tissue types and systematically evaluated the annotation accuracy under different conditions,including reference panels,sequencing depth,and feature selection strategies.Our results demonstrate that expanding the references is critical for improving annotation accuracy.Compared to many existing state-of-the-art annotation tools,deCS significantly reduced computation time and increased accuracy.deCS can be integrated into the standard scRNA-seq analytical pipeline to enhance cell type annotation.Finally,we demonstrated the broad utility of deCS to identify trait-cell type associations in 51 human complex traits,providing deep insights into the cellular mechanisms underlying disease pathogenesis.

关键词： Cell type-specific enrichment analysis scRNA-seq Cell type annotation Trait-cell type association Cell typemarkergene