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  1. Article ; Online: Isolation and Fluorescent Labeling of Extracellular Vesicles from Cultured Tumor Cells.

    Leary, Noelle / Walser, Sarina / Dieterich, Lothar C

    Methods in molecular biology (Clifton, N.J.)

    2022  Volume 2504, Page(s) 199–206

    Abstract: Extracellular vesicles (EVs), comprising exosomes, ectosomes, and apoptotic bodies, are an important component of molecular cell-to-cell communication, and are critically involved in the pathophysiology of various diseases, including tumors. In order to ... ...

    Abstract Extracellular vesicles (EVs), comprising exosomes, ectosomes, and apoptotic bodies, are an important component of molecular cell-to-cell communication, and are critically involved in the pathophysiology of various diseases, including tumors. In order to study the interaction of tumor cell-derived EVs with their target cells and to investigate their biological functions in comparison to other tumor cell-released factors, efficient isolation of EVs from cultured tumor cells, as well as fluorescent labeling of these EVs, is often necessary. In addition, EVs and EV-like particles are emerging as versatile vehicles for the delivery of therapeutic substances. Here, we describe an easy size exclusion chromatography-based method to isolate EVs from the mouse melanoma cell line B16F10 that yields highly enriched EV samples for subsequent applications such as molecular and functional studies. Our protocol also includes an optional labeling step with the lipophilic dye DiD, which allows tracking of EV uptake by recipient cells in vitro and in vivo.
    MeSH term(s) Animals ; Cell-Derived Microparticles ; Chromatography, Gel ; Exosomes ; Extracellular Vesicles/metabolism ; Mice ; Tumor Cells, Cultured
    Language English
    Publishing date 2022-04-25
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-2341-1_14
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  2. Article ; Online: Melanoma-derived extracellular vesicles mediate lymphatic remodelling and impair tumour immunity in draining lymph nodes.

    Leary, Noelle / Walser, Sarina / He, Yuliang / Cousin, Nikola / Pereira, Paulo / Gallo, Alessandro / Collado-Diaz, Victor / Halin, Cornelia / Garcia-Silva, Susana / Peinado, Hector / Dieterich, Lothar C

    Journal of extracellular vesicles

    2022  Volume 11, Issue 2, Page(s) e12197

    Abstract: Tumour-draining lymph nodes (LNs) undergo massive remodelling including expansion of the lymphatic sinuses, a process that has been linked to lymphatic metastasis by creation of a pre-metastatic niche. However, the signals leading to these changes have ... ...

    Abstract Tumour-draining lymph nodes (LNs) undergo massive remodelling including expansion of the lymphatic sinuses, a process that has been linked to lymphatic metastasis by creation of a pre-metastatic niche. However, the signals leading to these changes have not been completely understood. Here, we found that extracellular vesicles (EVs) derived from melanoma cells are rapidly transported by lymphatic vessels to draining LNs, where they selectively interact with lymphatic endothelial cells (LECs) as well as medullary sinus macrophages. Interestingly, uptake of melanoma EVs by LN-resident LECs was partly dependent on lymphatic VCAM-1 expression, and induced transcriptional changes as well as proliferation of those cells. Furthermore, melanoma EVs shuttled tumour antigens to LN LECs for cross-presentation on MHC-I, resulting in apoptosis induction in antigen-specific CD8
    MeSH term(s) CD8-Positive T-Lymphocytes ; Endothelial Cells/metabolism ; Extracellular Vesicles ; Humans ; Lymph Nodes ; Lymphatic Metastasis/pathology ; Lymphatic Vessels/pathology ; Melanoma/metabolism
    Language English
    Publishing date 2022-02-21
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2683797-3
    ISSN 2001-3078 ; 2001-3078
    ISSN (online) 2001-3078
    ISSN 2001-3078
    DOI 10.1002/jev2.12197
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  3. Article ; Online: Neurons burdened by DNA double-strand breaks incite microglia activation through antiviral-like signaling in neurodegeneration.

    Welch, Gwyneth M / Boix, Carles A / Schmauch, Eloi / Davila-Velderrain, Jose / Victor, Matheus B / Dileep, Vishnu / Bozzelli, P Lorenzo / Su, Qiao / Cheng, Jemmie D / Lee, Audrey / Leary, Noelle S / Pfenning, Andreas R / Kellis, Manolis / Tsai, Li-Huei

    Science advances

    2022  Volume 8, Issue 39, Page(s) eabo4662

    Abstract: DNA double-strand breaks (DSBs) are linked to neurodegeneration and senescence. However, it is not clear how DSB-bearing neurons influence neuroinflammation associated with neurodegeneration. Here, we characterize DSB-bearing neurons from the CK-p25 ... ...

    Abstract DNA double-strand breaks (DSBs) are linked to neurodegeneration and senescence. However, it is not clear how DSB-bearing neurons influence neuroinflammation associated with neurodegeneration. Here, we characterize DSB-bearing neurons from the CK-p25 mouse model of neurodegeneration using single-nucleus, bulk, and spatial transcriptomic techniques. DSB-bearing neurons enter a late-stage DNA damage response marked by nuclear factor κB (NFκB)-activated senescent and antiviral immune pathways. In humans, Alzheimer's disease pathology is closely associated with immune activation in excitatory neurons. Spatial transcriptomics reveal that regions of CK-p25 brain tissue dense with DSB-bearing neurons harbor signatures of inflammatory microglia, which is ameliorated by NFκB knockdown in neurons. Inhibition of NFκB in DSB-bearing neurons also reduces microglia activation in organotypic mouse brain slice culture. In conclusion, DSBs activate immune pathways in neurons, which in turn adopt a senescence-associated secretory phenotype to elicit microglia activation. These findings highlight a previously unidentified role for neurons in the mechanism of disease-associated neuroinflammation.
    MeSH term(s) Animals ; Antiviral Agents/metabolism ; DNA/metabolism ; DNA Breaks, Double-Stranded ; Humans ; Mice ; Microglia/metabolism ; NF-kappa B/metabolism ; Neurons/metabolism
    Chemical Substances Antiviral Agents ; NF-kappa B ; DNA (9007-49-2)
    Language English
    Publishing date 2022-09-28
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.abo4662
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  4. Article ; Online: Lipid accumulation induced by APOE4 impairs microglial surveillance of neuronal-network activity.

    Victor, Matheus B / Leary, Noelle / Luna, Xochitl / Meharena, Hiruy S / Scannail, Aine Ni / Bozzelli, P Lorenzo / Samaan, George / Murdock, Mitchell H / von Maydell, Djuna / Effenberger, Audrey H / Cerit, Oyku / Wen, Hsin-Lan / Liu, Liwang / Welch, Gwyneth / Bonner, Maeve / Tsai, Li-Huei

    Cell stem cell

    2022  Volume 29, Issue 8, Page(s) 1197–1212.e8

    Abstract: Apolipoprotein E4 (APOE4) is the greatest known genetic risk factor for developing sporadic Alzheimer's disease. How the interaction of APOE4 microglia with neurons differs from microglia expressing the disease-neutral APOE3 allele remains unknown. Here, ...

    Abstract Apolipoprotein E4 (APOE4) is the greatest known genetic risk factor for developing sporadic Alzheimer's disease. How the interaction of APOE4 microglia with neurons differs from microglia expressing the disease-neutral APOE3 allele remains unknown. Here, we employ CRISPR-edited induced pluripotent stem cells (iPSCs) to dissect the impact of APOE4 in neuron-microglia communication. Our results reveal that APOE4 induces a lipid-accumulated state that renders microglia weakly responsive to neuronal activity. By examining the transcriptional signatures of APOE3 versus APOE4 microglia in response to neuronal conditioned media, we established that neuronal cues differentially induce a lipogenic program in APOE4 microglia that exacerbates pro-inflammatory signals. Through decreased uptake of extracellular fatty acids and lipoproteins, we identified that APOE4 microglia disrupts the coordinated activity of neuronal ensembles. These findings suggest that abnormal neuronal network-level disturbances observed in Alzheimer's disease patients harboring APOE4 may in part be triggered by impairment in lipid homeostasis in non-neuronal cells.
    MeSH term(s) Alzheimer Disease ; Apolipoprotein E3/genetics ; Apolipoprotein E4/genetics ; Humans ; Microglia ; Neurons
    Chemical Substances Apolipoprotein E3 ; Apolipoprotein E4
    Language English
    Publishing date 2022-08-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2375354-7
    ISSN 1875-9777 ; 1934-5909
    ISSN (online) 1875-9777
    ISSN 1934-5909
    DOI 10.1016/j.stem.2022.07.005
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  5. Article ; Online: Multisensory gamma stimulation promotes glymphatic clearance of amyloid.

    Murdock, Mitchell H / Yang, Cheng-Yi / Sun, Na / Pao, Ping-Chieh / Blanco-Duque, Cristina / Kahn, Martin C / Kim, TaeHyun / Lavoie, Nicolas S / Victor, Matheus B / Islam, Md Rezaul / Galiana, Fabiola / Leary, Noelle / Wang, Sidney / Bubnys, Adele / Ma, Emily / Akay, Leyla A / Sneve, Madison / Qian, Yong / Lai, Cuixin /
    McCarthy, Michelle M / Kopell, Nancy / Kellis, Manolis / Piatkevich, Kiryl D / Boyden, Edward S / Tsai, Li-Huei

    Nature

    2024  Volume 627, Issue 8002, Page(s) 149–156

    Abstract: The glymphatic movement of fluid through the brain removes metabolic ... ...

    Abstract The glymphatic movement of fluid through the brain removes metabolic waste
    MeSH term(s) Animals ; Mice ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Alzheimer Disease/prevention & control ; Amyloid/metabolism ; Aquaporin 4/metabolism ; Astrocytes/metabolism ; Brain/cytology ; Brain/metabolism ; Brain/pathology ; Cerebrospinal Fluid/metabolism ; Disease Models, Animal ; Extracellular Fluid/metabolism ; Glymphatic System/physiology ; Interneurons/metabolism ; Vasoactive Intestinal Peptide/metabolism ; Cerebral Cortex/cytology ; Cerebral Cortex/metabolism ; Cerebral Cortex/pathology ; Gamma Rhythm ; Electric Stimulation
    Chemical Substances Amyloid ; Aquaporin 4 ; Vasoactive Intestinal Peptide (37221-79-7) ; Aqp4 protein, mouse
    Language English
    Publishing date 2024-02-28
    Publishing country England
    Document type Journal Article
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/s41586-024-07132-6
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    Zs.A 26: Show issues Location:
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  6. Article ; Online: Human microglial state dynamics in Alzheimer's disease progression.

    Sun, Na / Victor, Matheus B / Park, Yongjin P / Xiong, Xushen / Scannail, Aine Ni / Leary, Noelle / Prosper, Shaniah / Viswanathan, Soujanya / Luna, Xochitl / Boix, Carles A / James, Benjamin T / Tanigawa, Yosuke / Galani, Kyriaki / Mathys, Hansruedi / Jiang, Xueqiao / Ng, Ayesha P / Bennett, David A / Tsai, Li-Huei / Kellis, Manolis

    Cell

    2023  Volume 186, Issue 20, Page(s) 4386–4403.e29

    Abstract: Altered microglial states affect neuroinflammation, neurodegeneration, and disease but remain poorly understood. Here, we report 194,000 single-nucleus microglial transcriptomes and epigenomes across 443 human subjects and diverse Alzheimer's disease (AD) ...

    Abstract Altered microglial states affect neuroinflammation, neurodegeneration, and disease but remain poorly understood. Here, we report 194,000 single-nucleus microglial transcriptomes and epigenomes across 443 human subjects and diverse Alzheimer's disease (AD) pathological phenotypes. We annotate 12 microglial transcriptional states, including AD-dysregulated homeostatic, inflammatory, and lipid-processing states. We identify 1,542 AD-differentially-expressed genes, including both microglia-state-specific and disease-stage-specific alterations. By integrating epigenomic, transcriptomic, and motif information, we infer upstream regulators of microglial cell states, gene-regulatory networks, enhancer-gene links, and transcription-factor-driven microglial state transitions. We demonstrate that ectopic expression of our predicted homeostatic-state activators induces homeostatic features in human iPSC-derived microglia-like cells, while inhibiting activators of inflammation can block inflammatory progression. Lastly, we pinpoint the expression of AD-risk genes in microglial states and differential expression of AD-risk genes and their regulators during AD progression. Overall, we provide insights underlying microglial states, including state-specific and AD-stage-specific microglial alterations at unprecedented resolution.
    MeSH term(s) Humans ; Alzheimer Disease/genetics ; Alzheimer Disease/pathology ; Gene Expression Regulation ; Inflammation/pathology ; Microglia/metabolism ; Transcription Factors/metabolism ; Transcriptome ; Epigenome
    Chemical Substances Transcription Factors
    Language English
    Publishing date 2023-09-27
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2023.08.037
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  7. Article ; Online: Single-cell atlas reveals correlates of high cognitive function, dementia, and resilience to Alzheimer's disease pathology.

    Mathys, Hansruedi / Peng, Zhuyu / Boix, Carles A / Victor, Matheus B / Leary, Noelle / Babu, Sudhagar / Abdelhady, Ghada / Jiang, Xueqiao / Ng, Ayesha P / Ghafari, Kimia / Kunisky, Alexander K / Mantero, Julio / Galani, Kyriaki / Lohia, Vanshika N / Fortier, Gabrielle E / Lotfi, Yasmine / Ivey, Jason / Brown, Hannah P / Patel, Pratham R /
    Chakraborty, Nehal / Beaudway, Jacob I / Imhoff, Elizabeth J / Keeler, Cameron F / McChesney, Maren M / Patel, Haishal H / Patel, Sahil P / Thai, Megan T / Bennett, David A / Kellis, Manolis / Tsai, Li-Huei

    Cell

    2023  Volume 186, Issue 20, Page(s) 4365–4385.e27

    Abstract: Alzheimer's disease (AD) is the most common cause of dementia worldwide, but the molecular and cellular mechanisms underlying cognitive impairment remain poorly understood. To address this, we generated a single-cell transcriptomic atlas of the aged ... ...

    Abstract Alzheimer's disease (AD) is the most common cause of dementia worldwide, but the molecular and cellular mechanisms underlying cognitive impairment remain poorly understood. To address this, we generated a single-cell transcriptomic atlas of the aged human prefrontal cortex covering 2.3 million cells from postmortem human brain samples of 427 individuals with varying degrees of AD pathology and cognitive impairment. Our analyses identified AD-pathology-associated alterations shared between excitatory neuron subtypes, revealed a coordinated increase of the cohesin complex and DNA damage response factors in excitatory neurons and in oligodendrocytes, and uncovered genes and pathways associated with high cognitive function, dementia, and resilience to AD pathology. Furthermore, we identified selectively vulnerable somatostatin inhibitory neuron subtypes depleted in AD, discovered two distinct groups of inhibitory neurons that were more abundant in individuals with preserved high cognitive function late in life, and uncovered a link between inhibitory neurons and resilience to AD pathology.
    MeSH term(s) Aged ; Humans ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Brain/metabolism ; Brain/pathology ; Cognition ; Cognitive Dysfunction/metabolism ; Neurons/metabolism
    Language English
    Publishing date 2023-09-28
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2023.08.039
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