Could Galectin-3 be a key player in the etiology of neuromyelitis optica spectrum disorder?

Ramakrishnan, Pooja

doi:10.1016/j.mehy.2020.110450

Cited by 3 publications

(3 citation statements)

References 27 publications

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“…Microglia are the major mediators of CNS inflammation, and AQP4-IgG can induce cytokine production by activating astrocytes and lead to bystander activation towards microglia [28]. As one of the major antibody-mediated effects of NMOSD, microglial activation has both protective and disruptive effects, while the regulation of these two opposing effects remains to be further studied [29]. Chen et al indicate that with the involvement of complement, astrocyte-microglia crosstalk plays a critical role in promoting the development of NMO [30].…”

Section: Ivyspring International Publishermentioning

confidence: 99%

The role and mechanisms of Microglia in Neuromyelitis Optica Spectrum Disorders

Li¹,

Liu²,

Tan³

et al. 2021

Int. J. Med. Sci.

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Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune neurological disease that can cause blindness and disability. As the major mediators in the central nervous system, microglia plays key roles in immunological regulation in neuroinflammatory diseases, including NMOSD. Microglia can be activated by interleukin (IL)-6 and type I interferons (IFN-Is) during NMOSD, leading to signal transducer and activator of transcription (STAT) activation. Moreover, complement C3a secreted from activated astrocytes may induce the secretion of complement C1q, inflammatory cytokines and progranulin (PGRN) by microglia, facilitating injury to microglia, neurons, astrocytes and oligodendrocytes in an autocrine or paracrine manner. These processes involving activated microglia ultimately promote the pathological course of NMOSD. In this review, recent research progress on the roles of microglia in NMOSD pathogenesis is summarized, and the mechanisms of microglial activation and microglialmediated inflammation, and the potential research prospects associated with microglial activation are also discussed.

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Section: Ivyspring International Publishermentioning

confidence: 99%

The role and mechanisms of Microglia in Neuromyelitis Optica Spectrum Disorders

Li¹,

Liu²,

Tan³

et al. 2021

Int. J. Med. Sci.

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“…Recent singlecell transcriptomic studies of microglia have pointed to galectin 3 (Gal-3) as one of the most attractive molecules in brain innate immunity associated with neurodegeneration, such as Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS). 7,8 Analysis of the transcriptional profiles of the isolated microglia from the mouse models of AD and ALS has revealed a markedly upregulated Gal-3. 9 The candidate genes most likely to coordinate microglia activation phenotype have been also identified, including Lgals3, Igf l, Csf l, and Axl.…”

Section: ■ Introductionmentioning

confidence: 99%

“…Prion diseases include a group of fatal and transmissible neurodegenerative diseases that affect human beings and a variety of animals. , The typical neuropathological features were conformational converted PrP Sc deposit, spongiform degeneration, glial cell proliferation, and neuron loss, associated with neurotoxicity and neuroinflammation. , Activation of brain microglia cells is considered the main source of neuroinflammation. , With the advent of large-scale genomic analyses, conclusive evidence for the role of microglia in human neurodegeneration has been revealed. Recent single-cell transcriptomic studies of microglia have pointed to galectin 3 (Gal-3) as one of the most attractive molecules in brain innate immunity associated with neurodegeneration, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS). , Analysis of the transcriptional profiles of the isolated microglia from the mouse models of AD and ALS has revealed a markedly upregulated Gal-3 . The candidate genes most likely to coordinate microglia activation phenotype have been also identified, including Lgals3 , Igfl , Csfl , and Axl.…”

Section: Introductionmentioning

confidence: 99%

Increased Gal-3 Mediates Microglia Activation and Neuroinflammation via the TREM2 Signaling Pathway in Prion Infection

Fan,

Wu,

Jia

et al. 2023

ACS Chem. Neurosci.

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Galectin 3 (Gal-3) is one of the major elements for activating microglia and mediating neuroinflammation in some types of neurodegenerative diseases. However, its role in the pathogenesis of prion disease is seldom addressed. In this study, markedly increased brain Gal-3 was identified in three scrapie-infected rodent models at the terminal stage. The increased Gal-3 was mainly colocalized with the activated microglia. Coincidental with the increased brain Gal-3 in prion-infected animals, the expression of brain trigger receptor expressed in myeloid cell 2 (TREM2), one of the Gal-3 receptors, and some components in the downstream pathway also significantly increased, whereas Toll-like receptor 4 (TLR4), another Gal-3 receptor, and the main components in its downstream signaling were less changed. The increased Gal-3 signals were distributed at the areas with PrPSc deposit but looked not to colocalize directly with PrPSc/PrP signals. Similar changing profiles of Gal-3, the receptors TREM2 and TLR4, as well as the proteins in the downstream pathways were also observed in prion-infected cell line SMB-S15. Removal of PrPSc replication in SMB-S15 cells reversed the upregulation of cellular Gal-3, TREM2, and the relevant proteins. Moreover, we presented data for interactions of Gal-3 with TREM2 and with TLR4 morphologically and molecularly in the cultured cells. Stimulation of prion-infected cells or their normal partner cells with recombinant mouse Gal-3 in vitro induced obvious responses for activation of TREM2 signaling and TLR4 signaling. Our data here strongly indicate that prion infection or PrPSc deposit induces remarkably upregulated brain Gal-3, which is actively involved in the microglia activation and neuroinflammation mainly via TREM2 signaling.

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Research progress on pathogenesis and clinical treatment of neuromyelitis optica spectrum disorders (NMOSDs)

Shen

2023

Clinical Neurology and Neurosurgery

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Could Galectin-3 be a key player in the etiology of neuromyelitis optica spectrum disorder?

Cited by 3 publications

References 27 publications

The role and mechanisms of Microglia in Neuromyelitis Optica Spectrum Disorders

The role and mechanisms of Microglia in Neuromyelitis Optica Spectrum Disorders

Increased Gal-3 Mediates Microglia Activation and Neuroinflammation via the TREM2 Signaling Pathway in Prion Infection

Research progress on pathogenesis and clinical treatment of neuromyelitis optica spectrum disorders (NMOSDs)

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