Spatiotemporal expression patterns of Galectin-3 in perinatal rat hypoxic-ischemic brain injury model

Wang, Qian; Gao, Ruiwei; Wang, Minjie; Chen, Qiufan; Xiao, Mili; Liu, Zhihua; Wang, Laishuan; Chen, Chao

doi:10.1016/j.neulet.2019.134439

Cited by 5 publications

(10 citation statements)

References 24 publications

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“…Gal-3 has been demonstrated upregulates after perinatal white matter injury (PWMI) by our previous work and other studies, and Gal-3 has been detected co-stains with Iba-1, a marker of microglia (Chip et al, 2017 ; Stajic et al, 2019 ; Wang et al, 2019 ). Since Gal-3 knockdown causes neurodevelopmental retardation and demyelination, we wonder if exogenously Gal-3 administration is advantageous for myelin formation (Pasquini et al, 2011 ; Hoyos et al, 2014 ).…”

Section: Introductionmentioning

confidence: 76%

“…Our previous studies have demonstrated that Rice-Vanucci HI operation disrupts myelin formation and causes white matter injury (Huang et al, 2009 ; Wang et al, 2019 ). The PWMI model was performed as described preciously (Huang et al, 2009 ; Deng et al, 2015 ; Wang et al, 2019 ).…”

Section: Methodsmentioning

confidence: 99%

“…Throughout neurodevelopment, differentiation of oligodendrocyte linage is precisely controlled by extracellular and intrinsic signals (Sun et al, 2018 ; Elbaz and Popko, 2019 ). Galectin-3 (Gal-3), which is a carbohydrate-binding protein belonging to the lectin family (Dong et al, 2018 ; Wang et al, 2019 ). Gal-3 accelerates cell proliferation and differentiation, regulates cell-cell interactions within the extracellular matrix, modulates postnatal subventricular gliogenesis, and plays pleiotropic roles in central nervous system (CNS) (Hoyos et al, 2014 ; Chip et al, 2017 ; Dong et al, 2018 ; Kariya et al, 2018 ; Al-Dalahmah et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

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Galectin-3 administration drives remyelination after hypoxic-ischemic induced perinatal white matter injury

Wang

Diao²,

Qiu³

et al. 2022

Front. Cell. Neurosci.

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Hypoxic-ischemic (HI) induced perinatal white matter injury (PWMI) is a major cause of neurologic disabilities characterized by selective oligodendroglial death and myelin disruption. Galectin-3 (Gal-3) modulates postnatal subventricular zone gliogenesis and attenuates ischemic injury. However, the association between Gal-3 and myelin formation still remains unclear. In this study, we first perform Gal-3 knockdown (KD) to identify the importance of Gal-3 on myelin formation. Our results show impeded myelin formation, manifested by Olig2/CC1 (+) mature oligodendrocytes number, expression of oligodendroglial maturation-associated markers (MBP and CNPase), and myelin thickness and integrity. Then we perform recombinant Gal-3 (rGal-3) administration by intracerebroventricular injection. Notably, although rGal-3 administration shows no beneficial effect on oligodendrogenesis and myelin formation under normal condition, our results show that rGal-3 administration attenuates cognitive deficits and drives remyelination after PWMI, which are coupled to signs of enhanced myelin resiliency and cognition. Also, our results indicates that the significant increases in substrates for remyelination of rGal-3 administration are accompanied by enhanced Iba-1 (microglia marker)/ Mrc1 (M2 marker) (+) microglia and decreased Iba-1/ iNOS (M1 marker) (+) microglia. Altogether, our data in this research confirm the association between Gal-3 and myelin formation, underscore its position for the capacity for remyelination and restoration of function, and unveils the efficacy of rGal-3 administration with anti-inflammatory phenotype microglia (M2 microglia) activation. Thus, the findings suggest that Gal-3 plays a significant role in myelin formation and remyelination restoration.

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Section: Introductionmentioning

confidence: 76%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Galectin-3 administration drives remyelination after hypoxic-ischemic induced perinatal white matter injury

Wang

Diao²,

Qiu³

et al. 2022

Front. Cell. Neurosci.

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“…Galectin-3 is upregulated in both M1 and M2 type activated microglia (Figure 3B). Galectin-3 expression in microglia is enhanced by ischemic conditions or traumatic brain injury (Walther et al, 2000;Lalancette-Hébert et al, 2007;Yan et al, 2009;Venkatesan et al, 2010;Wesley et al, 2013;Yip et al, 2017;Rahimian et al, 2018;Wang et al, 2019). Treatment with trimethyltin, an organotin neurotoxicant, also induces galectin-3 expression in microglia and astrocytes in the hippocampal dentate gyrus (HDG) (Yang et al, 2012).…”

Section: Galectins In Glial Cells In the Cnsmentioning

confidence: 99%

Galectins and Their Ligand Glycoconjugates in the Central Nervous System Under Physiological and Pathological Conditions

Nio‐Kobayashi

Itabashi

2021

Front. Neuroanat.

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Galectins are β-galactoside-binding lectins consisting of 15 members in mammals. Galectin-1,-3,-4,-8, and -9 are predominantly expressed in the central nervous system (CNS) and regulate various physiological and pathological events. This review summarizes the current knowledge of the cellular expression and role of galectins in the CNS, and discusses their functions in neurite outgrowth, myelination, and neural stem/progenitor cell niches, as well as in ischemic/hypoxic/traumatic injuries and neurodegenerative diseases such as multiple sclerosis. Galectins are expressed in both neurons and glial cells. Galectin-1 is mainly expressed in motoneurons, whereas galectin-3-positive neurons are broadly distributed throughout the brain, especially in the hypothalamus, indicating its function in the regulation of homeostasis, stress response, and the endocrine/autonomic system. Astrocytes predominantly contain galectin-1, and galectin-3 and−9 are upregulated along with its activation. Activated, but not resting, microglia contain galectin-3, supporting its phagocytic activity. Galectin-1,−3, and -4 are characteristically expressed during oligodendrocyte differentiation. Galectin-3 from microglia promotes oligodendrocyte differentiation and myelination, while galectin-1 and axonal galectin-4 suppress its differentiation and myelination. Galectin-1- and- 3-positive cells are involved in neural stem cell niche formation in the subventricular zone and hippocampal dentate gyrus, and the migration of newly generated neurons and glial cells to the olfactory bulb or damaged lesions. In neurodegenerative diseases, galectin-1,-8, and -9 have neuroprotective and anti-inflammatory activities. Galectin-3 facilitates pro-inflammatory action; however, it also plays an important role during the recovery period. Several ligand glycoconjugates have been identified so far such as laminin, integrins, neural cell adhesion molecule L1, sulfatide, neuropilin-1/plexinA4 receptor complex, triggering receptor on myeloid cells 2, and T cell immunoglobulin and mucin domain. N-glycan branching on lymphocytes and oligodendroglial progenitors mediated by β1,6-N-acetylglucosaminyltransferase V (Mgat5/GnTV) influences galectin-binding, modulating inflammatory responses and remyelination in neurodegenerative diseases. De-sulfated galactosaminoglycans such as keratan sulfate are potential ligands for galectins, especially galectin-3, regulating neural regeneration. Galectins have multitudinous functions depending on cell type and context as well as post-translational modifications, including oxidization, phosphorylation, S-nitrosylation, and cleavage, but there should be certain rules in the expression patterns of galectins and their ligand glycoconjugates, possibly related to glucose metabolism in cells.

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“…In a rat model of perinatal hypoxic-ischemic brain injury, overexpression of Gal-3 by astrocytes, microglia, neurons and endotheliocytes was observed from 12 h post injury in various areas of the brain such as cortex, thalamus, corpus callosum and hippocampus ( Wang et al., 2019 ). LGALS3−/− mice show inhibited expression of IL-6, TNF-α, GABA-1 receptor subunits and brain-derived neurotrophic factor (BDNF) in the hippocampus, however lack of Gal-3 reduced LPS-induced neuroinflammation which decreased the anxiety of animals.…”

Section: Introductionmentioning

confidence: 99%

Galectins - Important players of the immune response to CNS parasitic infection

Maruszewska-Cheruiyot

Stear

Donskow‐Łysoniewska

2021

Brain, Behavior, & Immunity - Health

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Galectins are a family of proteins that bind β-galactosides and play key roles in a variety of cellular processes including host defense and entry of parasites into the host cells. They have been well studied in hosts but less so in parasites. As both host and parasite galectins are highly upregulated proteins following infection, galectins are an area of increasing interest and their role in immune modulation has only recently become clear. Correlation of CNS parasitic diseases with mental disorders as a result of direct or indirect interaction has been observed. Therefore, galectins produced by the parasite should be taken into consideration as potential therapeutic agents.

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Spatiotemporal expression patterns of Galectin-3 in perinatal rat hypoxic-ischemic brain injury model

Cited by 5 publications

References 24 publications

Galectin-3 administration drives remyelination after hypoxic-ischemic induced perinatal white matter injury

Galectin-3 administration drives remyelination after hypoxic-ischemic induced perinatal white matter injury

Galectins and Their Ligand Glycoconjugates in the Central Nervous System Under Physiological and Pathological Conditions

Galectins - Important players of the immune response to CNS parasitic infection

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