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Sodium nitrite prevents impaired postnatal alveolar development

American Journal of Physiology - Lung cellular and molecular Physiology 2025年第4期328卷 L586-L602页

作者： Daniel, Kathrine L. Gaudet, Chantal Hamraghani, Ali Fadel, Nadya Ben Yeganeh, Behzad Jankov, Robert P. Molecular Biomedicine Program Children’s Hospital of Eastern Ontario Research Institute Ottawa ON Canada Department of Paediatrics Faculty of Medicine University of Ottawa Ottawa ON Canada Department of Cellular and Molecular Medicine Faculty of Medicine University of Ottawa Ottawa ON Canada

Deficient nitric oxide (NO) signaling plays a critical role in the pathogenesis of bronchopulmonary dysplasia (BPD);however, clinical trials of inhaled NO (iNO) as a preventive therapy for BPD have shown little to no benefit. A biochemical obstacle to effective NO-based therapy relates to the high reactivity of NO, potentially leading to harmful oxidation and nitration. Hypothesizing that nitrite-based therapy has less potential to produce adverse reactions, we compared the preventive effects of sodium nitrite (NaNO₂) and iNO on lung morphology, NO content and signaling, S-nitrosothiols (SNOs), and tyrosine nitration in a novel rat model of experimental BPD. From postnatal days (PNDs) 1–21, rat pups were exposed to normoxia or to hyperoxia-intermittent hypoxia (H-IH;PND 1–7 85% O₂, PND 7–14 60% O₂, and PND 14–21 normoxia with intermittent exposure to 10% O₂ for 10 min every 4 h) while receiving daily subcutaneous (sc) NaNO₂ (20 mg/kg) or continuous iNO (10 ppm). Controls were treated with vehicle or were not exposed to iNO. Exposure to H-IH caused alveolar and pulmonary vascular hypoplasia, pulmonary hypertension (PH), decreased lung NO content and signaling, and increased tyrosine nitration. NaNO₂ prevented abnormal lung morphology and PH, normalized NO content and signaling, and prevented nitration. iNO prevented PH, but had minimal effects on abnormal distal airspace morphology, and caused nitration and alveolar hypoplasia in control (normoxia-exposed) animals. Treatment with NaNO₂ increased S-nitrosylation of nine lung proteins;none were increased by iNO. These observations provide a biological rationale for superior efficacy of NaNO₂ in preventing experimental BPD. Copyright © 2025 The Authors.

关键词： 3-nitrotyrosine nitric oxide S-nitrosylation serine-tRNA ligase xanthine oxidoreductase

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Proteostasis failure:at the intersection between aging and Alzheimer's disease

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Neural Regeneration Research 2025年第11期20卷 3221-3222页

作者： Natalia Poblete Claudio Hetz Center for Geroscience Brain Health and MetabolismSantiagoChile Biomedical Neuroscience Institute Faculty of MedicineUniversity of ChileSantiagoChile Program of Cellular and Molecular Biology Institute of Biomedical SciencesFaculty of MedicineUniversity of ChileSantiagoChile Buck Institute for Research on Aging NovatoCAUSA

Lifestyle and demographics of the world's population are causing serious health problems impacting the brain,increasing the incidence of Alzheimer's disease(AD)and other types of *** we have gained important insights into the pathogenic mechanisms of AD,only palliative care is available to *** is characterized by the abnormal deposition of protein aggregates in the brain formed by amyloid β and hyper-phosphorylated,Tau in addition to neuroinflammation.

关键词： Alzheimer amyloid stasis

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Tilting homeostatic and dyshomeostatic microglial balance in health and disease:transforming growth factor-beta1 as a critical protagonist

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Neural Regeneration Research 2025年第10期20卷 2895-2897页

作者： Nicolas Hugues Yu Luo Department of Molecular and Cellular Biosciences University of CincinnatiCincinnatiOHUSA Neuroscience Graduate Program University of CincinnatiCincinnatiOHUSA Division of Immunobiology Cincinnati Children’s Hospital Medical CenterUniversity of Cincinnati College of MedicineCincinnatiOHUSA

Adult microglia,by continuously sensing changes in their environment and communicating with nearly all brain cell types,are considered to be the immune sentinels of the *** the healthy central nervous system(CNS),microglia display a unique molecular homeostatic signature(i.e.,Tmem119,P2ry12,Sall1,Siglech,Gpr34,and Hexb)(Figure 1A).

关键词： Figure signature critical

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Invasion and metastasis in cancer:molecular insights and therapeutic targets

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Signal Transduction and Targeted Therapy 2025年第3期10卷 1503-1540页

作者： Yongxing Li Fengshuo Liu Qingjin Cai Lijun Deng Qin Ouyang Xiang H.-F.Zhang Ji Zheng Department of Urology Urologic Surgery CenterXinqiao HospitalThird Military Medical University(Army Medical University)ChongqingChina State Key Laboratory of Trauma and Chemical Poisoning Third Military Medical University(Army Medical University)ChongqingChina Lester and Sue Smith Breast Center Baylor College of MedicineHoustonTXUSA Dan L.Duncan Cancer Center Baylor College of MedicineHoustonTXUSA Department of Molecular and Cellular Biology Baylor College of MedicineHoustonTXUSA McNair Medical Institute Baylor College of MedicineHoustonTXUSA Graduate School of Biomedical Science Cancer and Cell Biology ProgramBaylor College of MedicineHoustonTXUSA Department of Medicinal Chemistry Third Military Medical University(Army Medical University)ChongqingChina

The progression of malignant tumors leads to the development of secondary tumors in various organs,including bones,the brain,liver,and *** metastatic process severely impacts the prognosis of patients,significantly affecting their quality of life and survival *** efforts have consistently focused on the intricate mechanisms underlying this process and the corresponding clinical management ***,a comprehensive understanding of the biological foundations of tumor metastasis,identification of pivotal signaling pathways,and systematic evaluation of existing and emerging therapeutic strategies are paramount to enhancing the overall diagnostic and treatment capabilities for metastatic ***,current research is primarily focused on metastasis within specific cancer types,leaving significant gaps in our understanding of the complex metastatic cascade,organ-specific tropism mechanisms,and the development of targeted *** this study,we examine the sequential processes of tumor metastasis,elucidate the underlying mechanisms driving organ-tropic metastasis,and systematically analyze therapeutic strategies for metastatic tumors,including those tailored to specific organ ***,we synthesize the most recent advances in emerging therapeutic technologies for tumor metastasis and analyze the challenges and opportunities encountered in clinical research pertaining to bone *** objective is to offer insights that can inform future research and clinical practice in this crucial field.

关键词： secondary tumors invasion metastatic process therapeutic targets molecular insights malignant tumors tumor metastasis metastasis

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Emerging Techniques in Spatial Multiomics: Fundamental Principles and Applications to Dermatology

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Journal of Investigative Dermatology 2025年第5期145卷 1017-1032页

作者： Jia, Bojing B. Sun, Bryan K. Lee, Ernest Y. Ren, Bing Bioinformatics and Systems Biology Graduate Program University of California San Diego La Jolla CA United States Medical Scientist Training Program University of California San Diego La Jolla CA United States Department of Dermatology University of California Irvine Irvine CA United States Department of Dermatology University of California San Francisco San Francisco CA United States Center for Epigenomics Department of Cellular & Molecular Medicine University of California San Diego La Jolla CA United States Institute of Genomic Medicine Moores Cancer Center School of Medicine University of California San Diego La Jolla CA United States

molecular pathology, such as high-throughput genomic and proteomic profiling, identifies precise disease targets from biopsies but require tissue dissociation, losing valuable histologic and spatial context. Emerging spatial multi-omic technologies now enable multiplexed visualization of genomic, proteomic, and epigenomic targets within a single tissue slice, eliminating the need for labeling multiple adjacent slices. Although early work focused on RNA (spatial transcriptomics), spatial technologies can now concurrently capture DNA, genome accessibility, histone modifications, and proteins with spatially-resolved single-cell resolution. This review outlines the principles, advantages, limitations, and potential for spatial technologies to advance dermatologic research. By jointly profiling multiple molecular channels, spatial multiomics enables novel studies of copy number variations, clonal heterogeneity, and enhancer dysregulation, replete with spatial context, illuminating the skin's complex heterogeneity. © 2024 The Authors

关键词： Dermatopathology Digital pathology Multiomics Multiplexed imaging Spatial sequencing

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An ovary-intact postmenopausal HFpEF mouse model;menopause is more than just estrogen deficiency

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American Journal of Physiology - Heart and Circulatory Physiology 2025年第4期328卷 H719-H733页

作者： Methawasin, Mei Strom, Joshua Marino, Vito A. Gohlke, Jochen Muldoon, Julia Herrick, Shelby R. van der Piji, Robbert Konhilas, John P. Granzier, Henk Department of Cellular and Molecular Medicine and Sarver Molecular Cardiovascular Research Program University of Arizona Tucson AZ United States Department of Medical Pharmacology and Physiology School of Medicine University of Missouri Columbia MO United States Department of Physiology and Sarver Molecular Cardiovascular Research Program University of Arizona Tucson AZ United States

The incidence of heart failure with preserved ejection fraction (HFpEF) in women significantly increases following menopause. This trend cannot solely be attributed to chronological aging, as evidenced by the more gradual increase in prevalence among men, suggesting that menopause is a provocative event for HFpEF. However, the underlying mechanisms remain elusive and challenging to investigate in human subjects;moreover, an attempt to create HFpEF in ovariectomized (OVX) mice was unsuccessful. In this study, we created an animal model that resembles HFpEF in women undergoing natural menopause. We used 4-vinylcyclohexene dioxide (VCD) to induce “ovary-intact” menopause, combined with the 2hit regimen (HFpEF inducing regimen) to model postmenopausal HFpEF. The female-VCD-2hit mice demonstrate diastolic dysfunction. At the left ventricle (LV) levels, the increased stiffness coefficient of end-diastolic pressure-volume relation (EDPVR), elevated LV end-diastolic pressure, and increased relaxation time constant indicate a heightened LV stiffness, delayed relaxation, and elevated LV filling pressure. At the cardiomyocyte level, the female-VCD-2hit mice exhibit increased cellular diastolic stiffness and delayed relaxation, suggesting that the observed LV dysfunction is derived from the cardiomyocytes. In addition, plasma N-terminal pro-b-type natriuretic peptide (NT-pro-BNP) levels were elevated, whereas Xbp1s transcript levels were reduced, further supporting the existence of HFpEF. Plasma-free testosterone was increased in VCD mice compared with premenopausal and OVX models. Further studies are required to determine whether the relative increase in testosterone is the factor driving HFpEF susceptibility in VCD mice. Ovary-intact postmenopausal status makes female mice vulnerable to HFpEF development. The VCD-2hit model develops a robust HFpEF-like phenotype and is suitable for studying female HFpEF. NEW & NOTEWORTHY Although ovariectomized mice were observed to be resist

关键词： diastolic dysfunction HFpEF ovary-intact menopause postmenopause

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New job for an old tool: PI3Kβ phosphorylates OGT to regulate acetyl-CoA in glioblastoma

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Trends in cell biology 2025年第5期35卷 361-363页

作者： Riley G Young Nusaiba N Ahmed Mauricio J Reginato Department of Biochemistry and Molecular Biology Drexel University College of Medicine Philadelphia PA USA. Department of Biochemistry and Molecular Biology Drexel University College of Medicine Philadelphia PA USA Translational and Cellular Oncology Program Sidney Kimmel Comprehensive Cancer Center Thomas Jefferson University Philadelphia PA USA. Electronic address: mjr53@drexel.edu.

Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta (PI3Kβ) is recognized for its role in cellular signaling as a lipid kinase. He and colleagues recently reported a non-canonical function of PI3Kβ where, under high glucose, it phosphorylates and activates O-GlcNAc transferase (OGT). This activation enhances ATP-citrate synthase (ACLY) O-GlcNAcylation, increasing acetyl-CoA production, fueling fatty acid metabolism and histone acetylation, and driving glioblastoma (GBM) growth.

关键词： ACLY HK1 O-GlcNAc transferase PI3Kβ acetyl-CoA acetylation glioblastoma kinase

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An innate drive to save a life

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Science (New York, N.Y.) 2025年第6736期387卷 827-828页

作者： William M Sheeran Zoe R Donaldson Department of Molecular Cellular and Developmental Biology University of Colorado Boulder Boulder CO USA. Medical Scientist Training Program University of Colorado School of Medicine Aurora CO USA. Department of Psychology and Neuroscience University of Colorado Boulder Boulder CO USA.

In mice, two brain regions drive the impulse to revive an unconscious companion.

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PTPσ-mediated PI3P regulation modulates neurodegeneration in C9ORF72-ALS/FTD

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Neuron 2025年第8期113卷 1190-1205.e9页

作者： Zhang, Zhe Fu, Xiujuan Wright, Noelle Wang, Weiren Ye, Yingzhi Asbury, Julie Li, Yini Zhu, Chengzhang Wu, Rong Wang, Shaopeng Sun, Shuying Department of Physiology Johns Hopkins University School of Medicine Baltimore 21205 MD United States Brain Science Institute Johns Hopkins University School of Medicine Baltimore 21205 MD United States Cellular and Molecular Physiology Graduate Program Johns Hopkins University School of Medicine Baltimore 21205 MD United States Biotechology Master Program Johns Hopkins University Baltimore 21205 MD United States Notre Dame of Maryland University Baltimore 21210 MD United States Cellular and Molecular Medicine Graduate Program Johns Hopkins University School of Medicine Baltimore 21205 MD United States The Solomon H. Snyder Department of Neuroscience and Department of Pathology Johns Hopkins University School of Medicine Baltimore 21205 MD United States

The most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is the repeat expansion in C9ORF72. Dipeptide repeat (DPR) proteins translated from both sense and antisense repeats, especially arginine-rich DPRs (R-DPRs), contribute to neurodegeneration. Through CRISPR interference (CRISPRi) screening in human-derived neurons, we identified receptor-type tyrosine-protein phosphatase S (PTPσ) as a strong modifier of poly-GR-mediated toxicity. We showed that reducing PTPσ promotes the survival of both poly-GR- and poly-PR-expressing neurons by elevating phosphatidylinositol 3-phosphate (PI3P), accompanied by restored early endosomes and lysosomes. Remarkably, PTPσ knockdown or inhibition substantially rescues the PI3P-endolysosomal defects and improves the survival of C9ORF72-ALS/FTD patient-derived neurons. Furthermore, the PTPσ inhibitor diminishes GR toxicity and rescues pathological and behavioral phenotypes in mice. Overall, these findings emphasize the critical role of PI3P-mediated endolysosomal deficits induced by R-DPRs in disease pathogenesis and reveal the therapeutic potential of targeting PTPσ in C9ORF72-ALS/FTD. © 2025 Elsevier Inc.

关键词： ALS C9ORF72 CRISPR screening endosome FTD lysosome PI3P poly-GR/PR PTPσ

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Highly multiplexed spatial transcriptomics in bacteria

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Science (New York, N.Y.) 2025年第6732期387卷 eadr0932页

作者： Sarfatis, Ari Wang, Yuanyou Twumasi-Ankrah, Nana Moffitt, Jeffrey R. Program in Cellular and Molecular Medicine Boston Children's Hospital Boston MA United States Department of Microbiology Harvard Medical School Boston MA United States Broad Institute of Harvard and MIT Cambridge MA United States

Single-cell decisions made in complex environments underlie many bacterial phenomena. Image-based transcriptomics approaches offer an avenue to study such behaviors, yet these approaches have been hindered by the massive density of bacterial messenger RNA. To overcome this challenge, we combined 1000-fold volumetric expansion with multiplexed error-robust fluorescence in situ hybridization (MERFISH) to create bacterial-MERFISH. This method enables high-throughput, spatially resolved profiling of thousands of operons within individual bacteria. Using bacterial-MERFISH, we dissected the response of Escherichia coli to carbon starvation, systematically mapped subcellular RNA organization, and charted the adaptation of a gut commensal Bacteroides thetaiotaomicron to micrometer-scale niches in the mammalian colon. We envision that bacterial-MERFISH will be broadly applicable to the study of bacterial single-cell heterogeneity in diverse, spatially structured, and native environments.

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