Translocator Protein Regulate Polarization Phenotype Transformation of Microglia after Cerebral Ischemia–reperfusion Injury

Yusuying, Shadamu; Yusuyin, Shalayiding; Cheng, Xiaojiang

doi:10.1016/j.neuroscience.2021.09.024

Cited by 7 publications

(6 citation statements)

References 74 publications

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“…M2 microglia mainly secrete anti-inflammatory factors, such as IL-10 and transforming growth factor-β (TGF-β), which exert their anti-inflammatory, repair, and regeneration effects [23] . Recent in vitro and in vivo studies revealed that bioactive natural products or drug molecules that promote microglial polarization from the M1 phenotype toward the M2 phenotype can significantly alleviate cerebral ischaemia‒reperfusion injury [ 24 , 25 ]. Our current study indicated that OGD/R activated microglia to transform from quiescent microglia to the proinflammatory M1 phenotype, thereby releasing a large amount of HMGB1 and proinflammatory cytokines (TNF-α, IL-1β, and IL-6).…”

Section: Discussionmentioning

confidence: 99%

Calycosin attenuates the inflammatory damage of microglia induced by oxygen and glucose deprivation through the HMGB1/TLR4/NF-κB signaling pathway

Li¹,

Yang²,

Lü³

et al. 2023

ABBS

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Stroke seriously threatens human life and health worldwide, but only very few effective stroke medicines are currently available. Our previous studies have indicated that the phytoestrogen calycosin exerts neuroprotective effects in cerebral ischemia and reperfusion injury rats. Therefore, the objective of this study is to further explore the protective effect of calycosin on inflammatory injury in microglia after oxygen-glucose deprivation/reoxygenation (OGD/R) and to clarify whether its protective effect is related to the HMGB1/TLR4/NF-κB signaling pathway. Here, the OGD/R model of rodent microglia is established in vitro to simulate cerebral ischemia-reperfusion injury. Through the CCK-8 test, ELISA, qRT-PCR, and western blot analysis, we find that the activity of microglia is decreased, the expressions of HMGB1 and TLR4 and the phosphorylation of NF-κB (p-NF-κB) are increased, and the releases of the inflammatory factors IL-6, IL-1β, and TNF-α are increased after OGD/R. Pretreatment with calycosin could ameliorate these states, increase cell viability, reduce HMGB1, TLR4 and p-NF-κB expression, and reduce inflammatory cytokine production. In addition, the effect of calycosin is similar to that of TAK-242 (an inhibitor of TLR4), and the effect of the combined treatment is better than that of the single treatment. The results indicate that calycosin protects microglia from OGD/R injury and reduces the inflammatory response. Calycosin might alleviate cerebral ischemia-reperfusion injury by inhibiting the HMGB1/TLR4/NF-κB pathway.

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Section: Discussionmentioning

confidence: 99%

Calycosin attenuates the inflammatory damage of microglia induced by oxygen and glucose deprivation through the HMGB1/TLR4/NF-κB signaling pathway

Li¹,

Yang²,

Lü³

et al. 2023

ABBS

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“…Hence it is abundantly expressed on antigen-presenting cells, including microglia, macrophages, dendritic cells, and B cells, and is upregulated in response to injury ( Louveau et al, 2015 ; Hellström Erkenstam et al, 2016 ). Remarkably, it is seen an increase in both CD86 + and CD206 + subsets among brain CD11b + cells, in models of traumatic brain injury, neonatal brain hypoxia-ischemia and cerebral ischemia-reperfusion ( Jin et al, 2012 ; Hellström Erkenstam et al, 2016 ; Bai et al, 2017 ; Yusuying et al, 2022 ).…”

Section: Antibody-mediated Identification Of Microglial Markersmentioning

confidence: 99%

Established and emerging techniques for the study of microglia: visualization, depletion, and fate mapping

Bobotis,

Halvorson,

Carrier

et al. 2024

Front. Cell. Neurosci.

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The central nervous system (CNS) is an essential hub for neuronal communication. As a major component of the CNS, glial cells are vital in the maintenance and regulation of neuronal network dynamics. Research on microglia, the resident innate immune cells of the CNS, has advanced considerably in recent years, and our understanding of their diverse functions continues to grow. Microglia play critical roles in the formation and regulation of neuronal synapses, myelination, responses to injury, neurogenesis, inflammation, and many other physiological processes. In parallel with advances in microglial biology, cutting-edge techniques for the characterization of microglial properties have emerged with increasing depth and precision. Labeling tools and reporter models are important for the study of microglial morphology, ultrastructure, and dynamics, but also for microglial isolation, which is required to glean key phenotypic information through single-cell transcriptomics and other emerging approaches. Strategies for selective microglial depletion and modulation can provide novel insights into microglia-targeted treatment strategies in models of neuropsychiatric and neurodegenerative conditions, cancer, and autoimmunity. Finally, fate mapping has emerged as an important tool to answer fundamental questions about microglial biology, including their origin, migration, and proliferation throughout the lifetime of an organism. This review aims to provide a comprehensive discussion of these established and emerging techniques, with applications to the study of microglia in development, homeostasis, and CNS pathologies.

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“…At the molecular level, mechanisms of neuroinflammation have been unraveled in the last few years by ex vivo transcriptomic comparisons of microglial subpopulations (or single cells) dissociated after micro-dissection of the damaged brain regions in experimental animal models of disease or injuries at critical stages, as compared to analogous samples coming from the respective controls. Microglia was purified from primary cell suspensions by fluorescence-activated cell sorter (FACS) using for instance CD11b-fluorescent immunolabeling, and subjected to RNA-sequencing ( Keren-Shaul et al, 2017 ; Krasemann et al, 2017 ; Madore et al, 2020 ; Masuda et al, 2020b ; Li et al, 2021 ; Liu et al, 2021 ; Lu et al, 2021 ; Muzio et al, 2021 ; Yusuying et al, 2021 ). The key results of these approaches are summarized in Table 1 to facilitate comparison between the different pathological contexts of neuroinflammation.…”

Section: Neuroinflammation: the Innate Immune Reaction Of The Central...mentioning

confidence: 99%

“… Summarized from (i) Li et al, 2021 ; Liu et al, 2021 ; Lu et al, 2021 ; Yusuying et al, 2021 (for ischemia-reperfusion), (ii) Keren-Shaul et al, 2017 ; Krasemann et al, 2017 ; Butovsky and Weiner, 2018 ; Madore et al, 2020 (for Alzheimer’disease and amyotrophic lateral sclerosis), (iii) Muzio et al, 2021 (for aging); (iv) Madore et al, 2020 ; Li et al, 2021 (for Parkinson’s disease). Bold-italic: messengers secreted by microglial cells.…”

Section: Neuroinflammation: the Innate Immune Reaction Of The Central...mentioning

confidence: 99%

Neuroinflammation: A Possible Link Between Chronic Vascular Disorders and Neurodegenerative Diseases

Moyse

Krantic

Djellouli

et al. 2022

Front. Aging Neurosci.

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Various age-related diseases involve systemic inflammation, i.e. a stereotyped series of acute immune system responses, and aging itself is commonly associated with low-grade inflammation or inflamm’aging. Neuroinflammation is defined as inflammation-like processes inside the central nervous system, which this review discusses as a possible link between cardiovascular disease-related chronic inflammation and neurodegenerative diseases. To this aim, neuroinflammation mechanisms are first summarized, encompassing the cellular effectors and the molecular mediators. A comparative survey of the best-known physiological contexts of neuroinflammation (neurodegenerative diseases and transient ischemia) reveals some common features such as microglia activation. The recently published transcriptomic characterizations of microglia have pointed a marker core signature among neurodegenerative diseases, but also unraveled the discrepancies with neuroinflammations related with acute diseases of vascular origin. We next review the links between systemic inflammation and neuroinflammation, beginning with molecular features of respective pro-inflammatory cells, i.e. macrophages and microglia. Finally, we point out a gap of knowledge concerning the atherosclerosis-related neuroinflammation, which is for the most surprising given that atherosclerosis is established as a major risk factor for neurodegenerative diseases.

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Translocator Protein Regulate Polarization Phenotype Transformation of Microglia after Cerebral Ischemia–reperfusion Injury

Cited by 7 publications

References 74 publications

Calycosin attenuates the inflammatory damage of microglia induced by oxygen and glucose deprivation through the HMGB1/TLR4/NF-κB signaling pathway

Calycosin attenuates the inflammatory damage of microglia induced by oxygen and glucose deprivation through the HMGB1/TLR4/NF-κB signaling pathway

Established and emerging techniques for the study of microglia: visualization, depletion, and fate mapping

Neuroinflammation: A Possible Link Between Chronic Vascular Disorders and Neurodegenerative Diseases

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Translocator Protein Regulate Polarization Phenotype Transformation of Microglia after Cerebral Ischemia–reperfusion Injury

Cited by 7 publications

References 74 publications

Calycosin attenuates the inflammatory damage of microglia induced by oxygen and glucose deprivation through the HMGB1/TLR4/NF-&kappa;B signaling pathway

Calycosin attenuates the inflammatory damage of microglia induced by oxygen and glucose deprivation through the HMGB1/TLR4/NF-&kappa;B signaling pathway

Established and emerging techniques for the study of microglia: visualization, depletion, and fate mapping

Neuroinflammation: A Possible Link Between Chronic Vascular Disorders and Neurodegenerative Diseases

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Resources

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Calycosin attenuates the inflammatory damage of microglia induced by oxygen and glucose deprivation through the HMGB1/TLR4/NF-κB signaling pathway

Calycosin attenuates the inflammatory damage of microglia induced by oxygen and glucose deprivation through the HMGB1/TLR4/NF-κB signaling pathway