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  1. Article ; Online: A novel long non-coding RNA, lnc-RNU12, influences the T-cell cycle via c-JUN and CCNL2 in rheumatoid arthritis.

    Mo, Xing-Bo / Sun, Yang-Hua / Wu, Long-Fei / He, Pei / Cao, Rong-Rong / Lu, Xin / Zhang, Yong-Hong / Deng, Fei-Yan / Lei, Shu-Feng

    Rheumatology (Oxford, England)

    2022  Volume 62, Issue 5, Page(s) 1955–1963

    Abstract: Objectives: Long non-coding RNAs (lncRNAs) play important roles in RA pathogenesis ... the expression of protein-coding genes related to the cell cycle and apoptosis (e.g. c-JUN, CCNL2, CDK6, MYC ... RNF40, PKM, VPS35, DNAJB6 and FLCN). Finally, c-JUN and CCNL2 were identified as target genes of lnc ...

    Abstract Objectives: Long non-coding RNAs (lncRNAs) play important roles in RA pathogenesis. However, specific lncRNAs that regulate gene expression in RA pathogenesis are poorly known. This study was undertaken to characterize a novel lncRNA (lnc-RNU12) that has a lower-than-normal expression level in RA patients.
    Methods: We performed initial genome-wide lncRNA microarray screening in peripheral blood mononuclear cells from 28 RA cases and 18 controls. Multiple methods were used to validate the detected associations between lncRNAs and RA. Furthermore, we identified the source and characteristics of the highlighted lncRNAs, detected the target genes, and determined the functional effect on immune cells through lncRNA knock-down in Jurkat T cell lines.
    Results: lnc-RNU12 was downregulated in peripheral blood mononuclear cells and T cell subtypes of RA patients and was genetically associated with RA risk. lnc-RNU12 mediates the effect of microbiome alterations on RA risk. Activation of T cells caused low expression of lnc-RNU12. Knock-down of lnc-RNU12 in Jurkat T cells caused cell cycle S-phase arrest and altered the expression of protein-coding genes related to the cell cycle and apoptosis (e.g. c-JUN, CCNL2, CDK6, MYC, RNF40, PKM, VPS35, DNAJB6 and FLCN). Finally, c-JUN and CCNL2 were identified as target genes of lnc-RNU12 at the mRNA and protein expression levels. RNA-binding protein immunoprecipitation assays verified the interaction between lnc-RNU12 and the two proteins (c-Jun and cyclin L2) in Jurkat cells.
    Conclusions: Our study suggested that lnc-RNU12 was involved in the pathogenesis of RA by influencing the T cell cycle by targeting c-JUN and CCNL2.
    MeSH term(s) Humans ; Arthritis, Rheumatoid ; Cell Cycle ; Cyclins ; HSP40 Heat-Shock Proteins ; Leukocytes, Mononuclear/metabolism ; Molecular Chaperones ; Nerve Tissue Proteins ; RNA, Long Noncoding/genetics ; T-Lymphocytes/metabolism ; Transcription Factors ; Proto-Oncogene Proteins c-jun/metabolism
    Chemical Substances CCNL2 protein, human ; Cyclins ; DNAJB6 protein, human ; HSP40 Heat-Shock Proteins ; Molecular Chaperones ; Nerve Tissue Proteins ; RNA, Long Noncoding ; Transcription Factors ; Proto-Oncogene Proteins c-jun
    Language English
    Publishing date 2022-09-26
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1464822-2
    ISSN 1462-0332 ; 1462-0324
    ISSN (online) 1462-0332
    ISSN 1462-0324
    DOI 10.1093/rheumatology/keac553
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  2. Article ; Online: Involvement of homodomain interacting protein kinase 2-c-Jun N-terminal kinase/c-Jun cascade in the long-term synaptic toxicity and cognition impairment induced by neonatal Sevoflurane exposure.

    Liang, Lirong / Xie, Rougang / Lu, Rui / Ma, Ruixue / Wang, Xiaoxia / Wang, Fengjuan / Liu, Bing / Wu, Shengxi / Wang, Yazhou / Zhang, Hui

    Journal of neurochemistry

    2020  Volume 154, Issue 4, Page(s) 372–388

    Abstract: ... its downstream c-Jun N-terminal kinase (JNK)/c-Jun signaling in the long-term toxicity of neonatal Sevoflurane ... decrease in long-term potentiation, reduction in spine density and activation of JNK/c-Jun induced ... about its pediatric application. The synaptic toxicity and mechanisms underlying its long-term cognition impairment ...

    Abstract Sevoflurane is one of the most widely used anesthetics with recent concerns rising about its pediatric application. The synaptic toxicity and mechanisms underlying its long-term cognition impairment remain unclear. In this study, we investigated the expression and roles of homeodomain interacting protein kinase 2 (HIPK2), a stress activating kinase involved in neuronal survival and synaptic plasticity, and its downstream c-Jun N-terminal kinase (JNK)/c-Jun signaling in the long-term toxicity of neonatal Sevoflurane exposure. Our data showed that neonatal Sevoflurane exposure results in impairment of memory, enhancement of anxiety, less number of excitatory synapses and lower levels of synaptic proteins in the hippocampus of adult rats without significant changes of hippocampal neuron numbers. Up-regulation of HIPK2 and JNK/c-Jun was observed in hippocampal granular neurons shortly after Sevoflurane exposure and persisted to adult. 5-((6-Oxo-5-(6-(piperazin-1-yl)pyridin-3-yl)-1,6-dihydropyridin-3-yl)methylene)thiazolidine-2,4-dione trifluoroacetate, antagonist of HIPK2, could significantly rescue the cognition impairment, decrease in long-term potentiation, reduction in spine density and activation of JNK/c-Jun induced by Sevoflurane. JNK antagonist SP600125 partially restored synapse development and cognitive function without affecting the expression of HIPK2. These data, in together, revealed a novel role of HIPK2-JNK/c-Jun signaling in the long-term synaptic toxicity and cognition impairment of neonatal Sevoflurane exposure, indicating HIPK2-JNK/c-Jun cascade as a potential target for reducing the synaptic toxicity of Sevoflurane. Cover Image for this issue: doi: 10.1111/jnc.14757.
    MeSH term(s) Anesthetics, Inhalation/toxicity ; Animals ; Animals, Newborn ; Cognitive Dysfunction/chemically induced ; Cognitive Dysfunction/metabolism ; Hippocampus/drug effects ; Hippocampus/metabolism ; JNK Mitogen-Activated Protein Kinases/drug effects ; JNK Mitogen-Activated Protein Kinases/metabolism ; Long-Term Potentiation/drug effects ; MAP Kinase Signaling System/drug effects ; Male ; Neurons/drug effects ; Neurons/metabolism ; Protein-Serine-Threonine Kinases/drug effects ; Protein-Serine-Threonine Kinases/metabolism ; Rats ; Rats, Sprague-Dawley ; Sevoflurane/toxicity ; Synapses/drug effects ; Synapses/metabolism
    Chemical Substances Anesthetics, Inhalation ; Sevoflurane (38LVP0K73A) ; HIPK2 protein, rat (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2020-01-19
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80158-6
    ISSN 1471-4159 ; 0022-3042 ; 1474-1644
    ISSN (online) 1471-4159
    ISSN 0022-3042 ; 1474-1644
    DOI 10.1111/jnc.14910
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  3. Article ; Online: Fucoxanthin Prevents Long-Term Administration l-DOPA-Induced Neurotoxicity through the ERK/JNK-c-Jun System in 6-OHDA-Lesioned Mice and PC12 Cells.

    Liu, Jingwangwei / Lu, Yujia / Tang, Min / Shao, Fanghao / Yang, Dongzi / Chen, Shuchang / Xu, Ziyi / Zhai, Leilei / Chen, Juanjuan / Li, Qian / Wu, Wei / Chen, Haimin

    Marine drugs

    2022  Volume 20, Issue 4

    Abstract: ... the adverse effects triggered by long-term l-DA administration in PD patients is unclear. In the present study ... in mitochondrial membrane potential, suppressing ROS over-expression, and inhibiting active of ERK/JNK-c-Jun system and expression ... of caspase-3 protein. These results were demonstrated by PD mice with long-term administration of l-DA ...

    Abstract As the most abundant marine carotenoid extracted from seaweeds, fucoxanthin is considered to have neuroprotective activity via its excellent antioxidant properties. Oxidative stress is regarded as an important starting factor for neuronal cell loss and necrosis, is one of the causes of Parkinson's disease (PD), and is considered to be the cause of adverse reactions caused by the current PD commonly used treatment drug levodopa (l-DA). Supplementation with antioxidants early in PD can effectively prevent neurodegeneration and inhibit apoptosis in dopaminergic neurons. At present, the effect of fucoxanthin in improving the adverse effects triggered by long-term l-DA administration in PD patients is unclear. In the present study, we found that fucoxanthin can reduce cytotoxicity and suppress the high concentration of l-DA (200 μM)-mediated cell apoptosis in the 6-OHDA-induced PC12 cells through improving the reduction in mitochondrial membrane potential, suppressing ROS over-expression, and inhibiting active of ERK/JNK-c-Jun system and expression of caspase-3 protein. These results were demonstrated by PD mice with long-term administration of l-DA showing enhanced motor ability after intervention with fucoxanthin. Our data indicate that fucoxanthin may prove useful in the treatment of PD patients with long-term l-DA administration.
    MeSH term(s) Animals ; Antioxidants/pharmacology ; Antioxidants/therapeutic use ; Humans ; Levodopa/toxicity ; Mice ; Neurotoxicity Syndromes/drug therapy ; Neurotoxicity Syndromes/prevention & control ; Oxidopamine/toxicity ; PC12 Cells ; Parkinson Disease/drug therapy ; Parkinson Disease/metabolism ; Rats ; Xanthophylls/pharmacology ; Xanthophylls/therapeutic use
    Chemical Substances Antioxidants ; Xanthophylls ; fucoxanthin (06O0TC0VSM) ; Levodopa (46627O600J) ; Oxidopamine (8HW4YBZ748)
    Language English
    Publishing date 2022-03-31
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2175190-0
    ISSN 1660-3397 ; 1660-3397
    ISSN (online) 1660-3397
    ISSN 1660-3397
    DOI 10.3390/md20040245
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  4. Book ; Online ; E-Book: Nonclassical ion channels in the nervous system

    Tian-le, Xu / Wu, Long-Jun

    (Methods in signal transduction series)

    2021  

    Abstract: Intro -- Half Title -- Series Page -- Title Page -- Copyright Page -- Contents -- Preface -- Editors -- Contributors -- 1. Endogenous Activation and Neurophysiological Functions of Acid-Sensing Ion Channels -- 1.1 Introduction -- 1.2 Endogenous ... ...

    Author's details edited by Tian-le Xu and Long-Jun Wu
    Series title Methods in signal transduction series
    Abstract Intro -- Half Title -- Series Page -- Title Page -- Copyright Page -- Contents -- Preface -- Editors -- Contributors -- 1. Endogenous Activation and Neurophysiological Functions of Acid-Sensing Ion Channels -- 1.1 Introduction -- 1.2 Endogenous Conditions That May Activate ASICs -- 1.2.1 Metabolic Production of Protons -- 1.2.1.1 Carbon Dioxide -- 1.2.1.2 Lactate -- 1.2.2 Acidification Niche and Proton Generators -- 1.2.2.1 Na+/H+ Exchangers (NHEs) -- 1.2.2.2 Hydrogen Voltage-Gated Channel 1 (Hv1) -- 1.2.2.3 Carbonic Anhydrases (CAs) -- 1.3 ASICs and Neurophysiological Functions -- 1.3.1 Synaptic Development -- 1.3.2 Synaptic Plasticity -- 1.3.3 Regional Specific Functions of ASICs -- 1.3.3.1 Amygdala -- 1.3.3.2 Retina -- 1.3.3.3 Dorsal Root Ganglia (DRG) -- 1.4 Summary and Outlook -- Acknowledgements -- References -- 2. Acid-Sensing Ion Channels and Synaptic Plasticity: A Revisit -- 2.1 Introduction -- 2.2 Protons and ASICs in Synaptic Transmission -- 2.2.1 Protons Act as a Neurotransmitter in Synaptic Signaling -- 2.2.2 Modulation of Synaptic Transmission by ASICs -- 2.3 ASIC1a in Synaptic Plasticity -- 2.3.1 ASIC1a in LTP -- 2.3.1.1 Hippocampus -- 2.3.1.2 Amygdala -- 2.3.1.3 ACC -- 2.3.2 ASIC1a in LTD -- 2.3.2.1 Hippocampus -- 2.3.2.2 Insular Cortex -- 2.4 ASICs in Synaptic Remodeling -- 2.5 Summary and Future Perspectives -- Acknowledgements -- References -- 3. Trimeric Scaffold Ligand-Gated Ion Channels -- 3.1 An Introduction of Trimeric Scaffold of Ligand-Gated Ion Channels (TS-LGICs) -- 3.2 Subunit Stoichiometry and Single Subunit Architecture of P2X Receptors and ASIC Channels -- 3.3 Ion Permeation Pathway of P2X Receptors and ASIC Channels -- 3.4 Ligand Recognitions of P2X Receptors and ASIC Channels -- 3.5 Coordinated Allostery During Channel Activation of P2X Receptors and ASIC Channels.
    Keywords Electronic books
    Language English
    Size 1 Online-Ressource (xiv, 413 Seiten), Illustrationen
    Publisher CRC Press
    Publishing place Boca Raton
    Publishing country United States
    Document type Book ; Online ; E-Book
    Remark Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
    HBZ-ID HT021025880
    ISBN 978-1-00-040374-9 ; 9780367623951 ; 9781003109266 ; 1-00-040374-2 ; 0367623951 ; 1003109268
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  5. Article ; Online: Fucoxanthin Prevents Long-Term Administration l -DOPA-Induced Neurotoxicity through the ERK/JNK-c-Jun System in 6-OHDA-Lesioned Mice and PC12 Cells

    Jingwangwei Liu / Yujia Lu / Min Tang / Fanghao Shao / Dongzi Yang / Shuchang Chen / Ziyi Xu / Leilei Zhai / Juanjuan Chen / Qian Li / Wei Wu / Haimin Chen

    Marine Drugs, Vol 20, Iss 4, p

    2022  Volume 245

    Abstract: ... the adverse effects triggered by long-term l -DA administration in PD patients is unclear. In the present ... in mitochondrial membrane potential, suppressing ROS over-expression, and inhibiting active of ERK/JNK-c-Jun system and expression ... of caspase-3 protein. These results were demonstrated by PD mice with long-term administration of l -DA ...

    Abstract As the most abundant marine carotenoid extracted from seaweeds, fucoxanthin is considered to have neuroprotective activity via its excellent antioxidant properties. Oxidative stress is regarded as an important starting factor for neuronal cell loss and necrosis, is one of the causes of Parkinson’s disease (PD), and is considered to be the cause of adverse reactions caused by the current PD commonly used treatment drug levodopa ( l -DA). Supplementation with antioxidants early in PD can effectively prevent neurodegeneration and inhibit apoptosis in dopaminergic neurons. At present, the effect of fucoxanthin in improving the adverse effects triggered by long-term l -DA administration in PD patients is unclear. In the present study, we found that fucoxanthin can reduce cytotoxicity and suppress the high concentration of l -DA (200 μM)-mediated cell apoptosis in the 6-OHDA-induced PC12 cells through improving the reduction in mitochondrial membrane potential, suppressing ROS over-expression, and inhibiting active of ERK/JNK-c-Jun system and expression of caspase-3 protein. These results were demonstrated by PD mice with long-term administration of l -DA showing enhanced motor ability after intervention with fucoxanthin. Our data indicate that fucoxanthin may prove useful in the treatment of PD patients with long-term l -DA administration.
    Keywords fucoxanthin ; antioxidant ; Parkinson’s disease ; ERK/JNK-c-Jun pathway ; Biology (General) ; QH301-705.5
    Subject code 610
    Language English
    Publishing date 2022-03-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: c-Jun N-terminal kinase (JNK)-dependent internalization and Rab5-dependent endocytic sorting mediate long-distance retrograde neuronal death induced by axonal BDNF-p75 signaling.

    Escudero, C A / Cabeza, C / Moya-Alvarado, G / Maloney, M T / Flores, C M / Wu, C / Court, F A / Mobley, W C / Bronfman, F C

    Scientific reports

    2019  Volume 9, Issue 1, Page(s) 6070

    Abstract: During the development of the sympathetic nervous system, signals from tropomyosin-related kinase receptors (Trks) and p75 neurotrophin receptors (p75) compete to regulate survival and connectivity. During this process, nerve growth factor (NGF)- TrkA ... ...

    Abstract During the development of the sympathetic nervous system, signals from tropomyosin-related kinase receptors (Trks) and p75 neurotrophin receptors (p75) compete to regulate survival and connectivity. During this process, nerve growth factor (NGF)- TrkA signaling in axons communicates NGF-mediated trophic responses in signaling endosomes. Whether axonal p75 signaling contributes to neuronal death and how signaling endosomes contribute to p75 signaling has not been established. Using compartmentalized sympathetic neuronal cultures (CSCGs) as a model, we observed that the addition of BDNF to axons increased the transport of p75 and induced death of sympathetic neurons in a dynein-dependent manner. In cell bodies, internalization of p75 required the activity of JNK, a downstream kinase mediating p75 death signaling in neurons. Additionally, the activity of Rab5, the key GTPase regulating early endosomes, was required for p75 death signaling. In axons, JNK and Rab5 were required for retrograde transport and death signaling mediated by axonal BDNF-p75 in CSCGs. JNK was also required for the proper axonal transport of p75-positive endosomes. Thus, our findings provide evidence that the activation of JNK by p75 in cell bodies and axons is required for internalization to a Rab5-positive signaling endosome and the further propagation of p75-dependent neuronal death signals.
    MeSH term(s) Animals ; Apoptosis/drug effects ; Axons/metabolism ; Brain-Derived Neurotrophic Factor/metabolism ; Cells, Cultured ; Endosomes/metabolism ; Female ; JNK Mitogen-Activated Protein Kinases/antagonists & inhibitors ; JNK Mitogen-Activated Protein Kinases/metabolism ; Male ; Nerve Tissue Proteins/metabolism ; Neurons/cytology ; Neurons/metabolism ; Neurons/pathology ; Primary Cell Culture ; Rats ; Receptor, trkA/metabolism ; Receptors, Growth Factor/metabolism ; Superior Cervical Ganglion/cytology ; rab5 GTP-Binding Proteins/metabolism
    Chemical Substances Bdnf protein, rat ; Brain-Derived Neurotrophic Factor ; Nerve Tissue Proteins ; Receptors, Growth Factor ; Ngfr protein, rat (136958-07-1) ; Receptor, trkA (EC 2.7.10.1) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; rab5 GTP-Binding Proteins (EC 3.6.5.2)
    Language English
    Publishing date 2019-04-15
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-019-42420-6
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  7. Article ; Online: c-Jun N-terminal kinase (JNK)-dependent internalization and Rab5-dependent endocytic sorting mediate long-distance retrograde neuronal death induced by axonal BDNF-p75 signaling

    C. A. Escudero / C. Cabeza / G. Moya-Alvarado / M. T. Maloney / C. M. Flores / C. Wu / F. A. Court / W. C. Mobley / F. C. Bronfman

    Scientific Reports, Vol 9, Iss 1, Pp 1-

    2019  Volume 17

    Abstract: Abstract During the development of the sympathetic nervous system, signals from tropomyosin-related kinase receptors (Trks) and p75 neurotrophin receptors (p75) compete to regulate survival and connectivity. During this process, nerve growth factor (NGF)- ...

    Abstract Abstract During the development of the sympathetic nervous system, signals from tropomyosin-related kinase receptors (Trks) and p75 neurotrophin receptors (p75) compete to regulate survival and connectivity. During this process, nerve growth factor (NGF)- TrkA signaling in axons communicates NGF-mediated trophic responses in signaling endosomes. Whether axonal p75 signaling contributes to neuronal death and how signaling endosomes contribute to p75 signaling has not been established. Using compartmentalized sympathetic neuronal cultures (CSCGs) as a model, we observed that the addition of BDNF to axons increased the transport of p75 and induced death of sympathetic neurons in a dynein-dependent manner. In cell bodies, internalization of p75 required the activity of JNK, a downstream kinase mediating p75 death signaling in neurons. Additionally, the activity of Rab5, the key GTPase regulating early endosomes, was required for p75 death signaling. In axons, JNK and Rab5 were required for retrograde transport and death signaling mediated by axonal BDNF-p75 in CSCGs. JNK was also required for the proper axonal transport of p75-positive endosomes. Thus, our findings provide evidence that the activation of JNK by p75 in cell bodies and axons is required for internalization to a Rab5-positive signaling endosome and the further propagation of p75-dependent neuronal death signals.
    Keywords Medicine ; R ; Science ; Q
    Subject code 571 ; 572
    Language English
    Publishing date 2019-04-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: Tuning neural circuits and behaviors by microglia in the adult brain.

    Zhao, Shunyi / Umpierre, Anthony D / Wu, Long-Jun

    Trends in neurosciences

    2024  Volume 47, Issue 3, Page(s) 181–194

    Abstract: Microglia are the primary immune cells of the CNS, contributing to both inflammatory damage and tissue repair in neurological disorder. In addition, emerging evidence highlights the role of homeostatic microglia in regulating neuronal activity, ... ...

    Abstract Microglia are the primary immune cells of the CNS, contributing to both inflammatory damage and tissue repair in neurological disorder. In addition, emerging evidence highlights the role of homeostatic microglia in regulating neuronal activity, interacting with synapses, tuning neural circuits, and modulating behaviors. Herein, we review how microglia sense and regulate neuronal activity through synaptic interactions, thereby directly engaging with neural networks and behaviors. We discuss current studies utilizing microglial optogenetic and chemogenetic approaches to modulate adult neural circuits. These manipulations of microglia across different CNS regions lead to diverse behavioral consequences. We propose that spatial heterogeneity of microglia-neuron interaction lays the groundwork for understanding diverse functions of microglia in neural circuits and behaviors.
    MeSH term(s) Humans ; Microglia/physiology ; Brain/physiology ; Synapses/physiology ; Neurons/physiology ; Nervous System Diseases ; Neuronal Plasticity/physiology
    Language English
    Publishing date 2024-01-19
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 282488-7
    ISSN 1878-108X ; 0378-5912 ; 0166-2236
    ISSN (online) 1878-108X
    ISSN 0378-5912 ; 0166-2236
    DOI 10.1016/j.tins.2023.12.003
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  9. Article: Chemogenetic activation of microglial Gi signaling decreases microglial surveillance and impairs neuronal synchronization.

    Zhao, Shunyi / Wang, Lingxiao / Liang, Yue / Zheng, Jiaying / Umpierre, Anthony D / Wu, Long-Jun

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Microglia actively survey the brain and dynamically interact with neurons to maintain brain homeostasis. Microglial Gi-protein coupled receptors (Gi-GPCRs) play a critical role in microglia-neuron communications. However, the impact of temporally ... ...

    Abstract Microglia actively survey the brain and dynamically interact with neurons to maintain brain homeostasis. Microglial Gi-protein coupled receptors (Gi-GPCRs) play a critical role in microglia-neuron communications. However, the impact of temporally activating microglial Gi signaling on microglial dynamics and neuronal activity in the homeostatic brain remains largely unknown. In this study, we employed Gi-based Designer Receptors Exclusively Activated by Designer Drugs (Gi-DREADD) to selectively and temporally modulate microglial Gi signaling pathway. By integrating this chemogenetic approach with
    Language English
    Publishing date 2024-02-12
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.02.12.579861
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  10. Article ; Online: Getting a Sense of ATP in Real Time.

    Umpierre, Anthony D / Haruwaka, Koichiro / Wu, Long-Jun

    Neuroscience bulletin

    2022  Volume 38, Issue 7, Page(s) 834–836

    MeSH term(s) Adenosine Triphosphate
    Chemical Substances Adenosine Triphosphate (8L70Q75FXE)
    Language English
    Publishing date 2022-03-30
    Publishing country Singapore
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2419741-5
    ISSN 1995-8218 ; 1673-7067
    ISSN (online) 1995-8218
    ISSN 1673-7067
    DOI 10.1007/s12264-022-00846-5
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