Francisca Barake1,2, Andrea Soza1,2, Alfonso González1,2,3. 1. Centro de Biología Celular y Biomedicina (CEBICEM), Facultad de Medicina y Ciencia, Universidad San Sebastián. 2. Centro de Envejecimiento y Regeneración (CARE), Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile. 3. Fundación Ciencia y Vida, Santiago, Chile.
Abstract
PURPOSE OF REVIEW: Galectin interactions with glycoproteins and glycolipids modulate a variety of cellular responses that are now increasingly explored to better understand neuroinflammation processes and eventually find new therapeutic opportunities for neurological diseases. RECENT FINDINGS: Gal-1 confirmed its indirect neuroprotective roles through anti-inflammatory properties whereas Gal-3 remains elusive, showing anti-inflammatory or pro-inflammatory roles depending on damaging conditions and genetic background of mice models. Interestingly, microglial intracellular rather than extracellular overexpression of Gal-3 arose as contributing to the pathogenesis of Huntington disease, involving NLRP3 inflammasome activation and inhibition of autophagic removal of damaged endolysosomes. Decreasing Gal-3 expression had favorable effects upon disease symptoms. Gal-3 expanded its role in this endolysosomal surveillance system originally involving Gal-8 and Gal-9, which protect cells against neuropathogenic proteins and becomes impaired or even detrimental under neurodegenerative conditions. Also, Gal-1, Gal-3 and Gal-4, together with changes in glycan structures define the outcome of neuroinflammation and remyelination processes. Gal-8 emerged as a new neuroprotector factor, which added to its immunosuppressive role and presence in human cerebrospinal fluid (CSF) may generate a neuroprotective environment in the brain. SUMMARY: Galectins modulate neuroinflammation and neurodegenerative processes contributing to microglia polarization, immunosurveillance and neuroprotection through extracellular and intracellular interactions with particular and dynamic patterns of glycans, suggesting potential therapeutic targets.
PURPOSE OF REVIEW: Galectin interactions with glycoproteins and glycolipids modulate a variety of cellular responses that are now increasingly explored to better understand neuroinflammation processes and eventually find new therapeutic opportunities for neurological diseases. RECENT FINDINGS:Gal-1 confirmed its indirect neuroprotective roles through anti-inflammatory properties whereas Gal-3 remains elusive, showing anti-inflammatory or pro-inflammatory roles depending on damaging conditions and genetic background of mice models. Interestingly, microglial intracellular rather than extracellular overexpression of Gal-3 arose as contributing to the pathogenesis of Huntington disease, involving NLRP3 inflammasome activation and inhibition of autophagic removal of damaged endolysosomes. Decreasing Gal-3 expression had favorable effects upon disease symptoms. Gal-3 expanded its role in this endolysosomal surveillance system originally involving Gal-8 and Gal-9, which protect cells against neuropathogenic proteins and becomes impaired or even detrimental under neurodegenerative conditions. Also, Gal-1, Gal-3 and Gal-4, together with changes in glycan structures define the outcome of neuroinflammation and remyelination processes. Gal-8 emerged as a new neuroprotector factor, which added to its immunosuppressive role and presence in human cerebrospinal fluid (CSF) may generate a neuroprotective environment in the brain. SUMMARY: Galectins modulate neuroinflammation and neurodegenerative processes contributing to microglia polarization, immunosurveillance and neuroprotection through extracellular and intracellular interactions with particular and dynamic patterns of glycans, suggesting potential therapeutic targets.
Authors: Eleazar Ramírez Hernández; Beatriz Alanis Olvera; Daniela Carmona González; Oscar Guerrero Marín; Denisse Pantoja Mercado; Lucero Valencia Gil; Luis F Hernández-Zimbrón; José Luis Sánchez Salgado; I Daniel Limón; Edgar Zenteno Journal: Glycoconj J Date: 2022-06-02 Impact factor: 3.009
Authors: Juan García-Revilla; Antonio Boza-Serrano; Ana M Espinosa-Oliva; Manuel Sarmiento Soto; Tomas Deierborg; Rocío Ruiz; Rocío M de Pablos; Miguel Angel Burguillos; Jose L Venero Journal: Cell Death Dis Date: 2022-07-20 Impact factor: 9.685