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Keywords {🔍}

mice, mitochondrial, pubmed, mitophagy, microglial, mntreated, cells, fig, article, exposure, neuroinflammation, levels, google, scholar, analysis, pretreatment, cell, cas, dysfunction, group, disease, pathway, mninduced, central, data, excessive, activation, damage, compared, signaling, cgassting, role, manganese, control, assay, function, microglia, increased, neuroinflammatory, increase, wang, parkinsons, inflammatory, dna, liu, vivo, results, microgliamediated, expression, findings,

Topics {✒️}

microglial cgas-sting/nf-κb pathway gln-glu-gaba metabolic cycle mtdna/cyclic gmp-amp synthase mrna demethylase fto pink1/parkin-mediated mitophagy changed repressing pink1/parkin-mediated mitophagy sds-page gels manganese induces s-nitrosylation cyclic gmp-amp synthase microglial pink1/parkin-mediated mitophagy pink1/parkin-mediated mitophagy contributes pink1/parkin-mediated mitophagy pathway single-nucleus rna-sequencing pink1/parkin-mediated mitophagy due mn-induced neurocytes injury cyclic dinucleotide-manganese particles sirt1-pgc1α signaling pathway bmc pharmacol toxicol enzyme-linked immunoassay analyzer sn-rna sequencing analysis manganese-induced nerve damage manganese ethylene-bis-dithiocarbamate high energy-demanding tissues enzyme-linked immunosorbent assay microglia-mediated neuroinflammatory injury mn-induced neuroinflammatory damage microglial cgas-sting signaling mn-induced neurological dysfunction microglial-mediated neuroinflammation plays microglial cgas-sting activity microglial cgas-sting pathway exogenous double-stranded dna cgas-sting activity score cgas-sting pathway modulators cgas/sting signaling pathway cgas-sting signaling pathway alleviates neurobehavioral impairments microglia m1/m2 polarization mn-treated bv2 cells alleviate mn-induced neuroinflammation mtdna-sting pathway requires rab10-mediated autophagy dysfunction central nervous system microglia-mediated neuroinflammatory damage multimodal single-cell data mn-induced mitochondrial dysfunction mtdna-sting signaling pathway mn-treated group compared annotated interferon-regulated genes cgas-sting signaling activation

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         headline:Protective role of mitophagy on microglia-mediated neuroinflammatory injury through mtDNA-STING signaling in manganese-induced parkinsonism
         description:Manganese (Mn), the third most abundant transition metal in the earth’s crust, has widespread applications in the emerging field of organometallic catalysis and traditional industries. Excessive Mn exposure causes neurological syndrome resembling Parkinson’s disease (PD). The pathogenesis of PD is thought to involve microglia-mediated neuroinflammatory injury, with mitochondrial dysfunction playing a role in aberrant microglial activation. In the early stages of PD, PINK1/Parkin-mediated mitophagy contributes to the microglial inflammatory response via the cGAS/STING signaling pathway. Suppression of PINK1/Parkin-mediated mitophagy due to excessive Mn exposure exacerbates neuronal injury. Moreover, excessive Mn exposure leads to neuroinflammatory damage via the microglial cGAS-STING pathway. However, the precise role of microglial mitophagy in modulating neuroinflammation in Mn-induced parkinsonism and its underlying molecular mechanism remains unclear. Here, we observed that Mn-exposed mice exhibited neurobehavioral abnormalities and detrimental microglial activation, along with increased apoptosis of nerve cells, proinflammatory cytokines, and intracellular ROS. Furthermore, in vivo and in vitro experiments showed that excessive Mn exposure resulted in microglial mitochondrial dysfunction, manifested by increased mitochondrial ROS, decreased mitochondrial mass, and membrane potential. Additionally, with the escalating Mn dose, PINK1/Parkin-mediated mitophagy changed from activation to suppression. This was evidenced by decreased levels of LC3-II, PINK1, p-Parkin/Parkin, and increased levels of p62 protein expression level, as well as the colocalization between ATPB and LC3B due to excessive Mn exposure. Upregulation of mitophagy by urolithin A could mitigate Mn-induced mitochondrial dysfunction, as indicated by decreased mitochondrial ROS, increased mitochondrial mass, and membrane potential, along with improvements in neurobehavioral deficits and attenuated detrimental microglial activation. Using single-nucleus RNA-sequencing (snRNA-seq) analysis in the Mn-exposed mouse model, we identified the microglial cGAS-STING signaling pathway as a potential mechanism underlying Mn-induced neuroinflammation. This pathway is associated with an increase in cytosolic mtDNA levels, which activate STING signaling. These findings point to the induction of microglial mitophagy as a viable strategy to alleviate Mn-induced neuroinflammation through mtDNA-STING signaling.
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      headline:Protective role of mitophagy on microglia-mediated neuroinflammatory injury through mtDNA-STING signaling in manganese-induced parkinsonism
      description:Manganese (Mn), the third most abundant transition metal in the earth’s crust, has widespread applications in the emerging field of organometallic catalysis and traditional industries. Excessive Mn exposure causes neurological syndrome resembling Parkinson’s disease (PD). The pathogenesis of PD is thought to involve microglia-mediated neuroinflammatory injury, with mitochondrial dysfunction playing a role in aberrant microglial activation. In the early stages of PD, PINK1/Parkin-mediated mitophagy contributes to the microglial inflammatory response via the cGAS/STING signaling pathway. Suppression of PINK1/Parkin-mediated mitophagy due to excessive Mn exposure exacerbates neuronal injury. Moreover, excessive Mn exposure leads to neuroinflammatory damage via the microglial cGAS-STING pathway. However, the precise role of microglial mitophagy in modulating neuroinflammation in Mn-induced parkinsonism and its underlying molecular mechanism remains unclear. Here, we observed that Mn-exposed mice exhibited neurobehavioral abnormalities and detrimental microglial activation, along with increased apoptosis of nerve cells, proinflammatory cytokines, and intracellular ROS. Furthermore, in vivo and in vitro experiments showed that excessive Mn exposure resulted in microglial mitochondrial dysfunction, manifested by increased mitochondrial ROS, decreased mitochondrial mass, and membrane potential. Additionally, with the escalating Mn dose, PINK1/Parkin-mediated mitophagy changed from activation to suppression. This was evidenced by decreased levels of LC3-II, PINK1, p-Parkin/Parkin, and increased levels of p62 protein expression level, as well as the colocalization between ATPB and LC3B due to excessive Mn exposure. Upregulation of mitophagy by urolithin A could mitigate Mn-induced mitochondrial dysfunction, as indicated by decreased mitochondrial ROS, increased mitochondrial mass, and membrane potential, along with improvements in neurobehavioral deficits and attenuated detrimental microglial activation. Using single-nucleus RNA-sequencing (snRNA-seq) analysis in the Mn-exposed mouse model, we identified the microglial cGAS-STING signaling pathway as a potential mechanism underlying Mn-induced neuroinflammation. This pathway is associated with an increase in cytosolic mtDNA levels, which activate STING signaling. These findings point to the induction of microglial mitophagy as a viable strategy to alleviate Mn-induced neuroinflammation through mtDNA-STING signaling.
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               type:PostalAddress
            type:Organization
      name:Jie Wu
      affiliation:
            name:Jinzhou Medical University
            address:
               name:School of Public Health, Jinzhou Medical University, Jinzhou, China
               type:PostalAddress
            type:Organization
      name:Jia Meng
      affiliation:
            name:Jinzhou Medical University
            address:
               name:School of Public Health, Jinzhou Medical University, Jinzhou, China
               type:PostalAddress
            type:Organization
            name:Collaborative Innovation Center For Health Promotion of Children and Adolescents of Jinzhou Medical University
            address:
               name:Collaborative Innovation Center For Health Promotion of Children and Adolescents of Jinzhou Medical University, Jinzhou, China
               type:PostalAddress
            type:Organization
      name:Hong Li
      affiliation:
            name:Jinzhou Medical University
            address:
               name:School of Public Health, Jinzhou Medical University, Jinzhou, China
               type:PostalAddress
            type:Organization
            name:Collaborative Innovation Center For Health Promotion of Children and Adolescents of Jinzhou Medical University
            address:
               name:Collaborative Innovation Center For Health Promotion of Children and Adolescents of Jinzhou Medical University, Jinzhou, China
               type:PostalAddress
            type:Organization
      name:Dongying Yan
      url:https://orcid.org/0000-0002-9201-8237
      affiliation:
            name:Jinzhou Medical University
            address:
               name:School of Public Health, Jinzhou Medical University, Jinzhou, China
               type:PostalAddress
            type:Organization
            name:Collaborative Innovation Center For Health Promotion of Children and Adolescents of Jinzhou Medical University
            address:
               name:Collaborative Innovation Center For Health Promotion of Children and Adolescents of Jinzhou Medical University, Jinzhou, China
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:School of Public Health, Jinzhou Medical University, Jinzhou, China
      name:School of Public Health, Jinzhou Medical University, Jinzhou, China
      name:Collaborative Innovation Center For Health Promotion of Children and Adolescents of Jinzhou Medical University, Jinzhou, China
      name:School of Public Health, Jinzhou Medical University, Jinzhou, China
      name:School of Public Health, Jinzhou Medical University, Jinzhou, China
      name:School of Public Health, Jinzhou Medical University, Jinzhou, China
      name:School of Public Health, Jinzhou Medical University, Jinzhou, China
      name:School of Public Health, Jinzhou Medical University, Jinzhou, China
      name:School of Public Health, Jinzhou Medical University, Jinzhou, China
      name:School of Public Health, Jinzhou Medical University, Jinzhou, China
      name:Collaborative Innovation Center For Health Promotion of Children and Adolescents of Jinzhou Medical University, Jinzhou, China
      name:School of Public Health, Jinzhou Medical University, Jinzhou, China
      name:Collaborative Innovation Center For Health Promotion of Children and Adolescents of Jinzhou Medical University, Jinzhou, China
      name:School of Public Health, Jinzhou Medical University, Jinzhou, China
      name:Collaborative Innovation Center For Health Promotion of Children and Adolescents of Jinzhou Medical University, Jinzhou, China

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