{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["10(1)"],"submitter":["Siew JJ"],"pubmed_abstract":["Huntington's disease (HD) is a neurodegenerative disorder that manifests with movement dysfunction. The expression of mutant Huntingtin (mHTT) disrupts the functions of brain cells. Galectin-3 (Gal3) is a lectin that has not been extensively explored in brain diseases. Herein, we showed that the plasma Gal3 levels of HD patients and mice correlated with disease severity. Moreover, brain Gal3 levels were higher in patients and mice with HD than those in controls. The up-regulation of Gal3 in HD mice occurred before motor impairment, and its level remained high in microglia throughout disease progression. The cell-autonomous up-regulated Gal3 formed puncta in damaged lysosomes and contributed to inflammation through NFκB- and NLRP3 inflammasome-dependent pathways. Knockdown of Gal3 suppresse"],"journal":["Nature communications"],"pagination":["3473"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6677843"],"repository":["biostudies-literature"],"pubmed_title":["Galectin-3 is required for the microglia-mediated brain inflammation in a model of Huntington's disease."],"pmcid":["PMC6677843"],"pubmed_authors":["Chang CP","Wu YR","Soong BW","Chen CM","Chen HY","Chan YC","Liu FT","Chern Y","Chen HM","Chen HL","Lin CH","Siew JJ"],"additional_accession":[]},"is_claimable":false,"name":"Galectin-3 is required for the microglia-mediated brain inflammation in a model of Huntington's disease.","description":"Huntington's disease (HD) is a neurodegenerative disorder that manifests with movement dysfunction. The expression of mutant Huntingtin (mHTT) disrupts the functions of brain cells. Galectin-3 (Gal3) is a lectin that has not been extensively explored in brain diseases. Herein, we showed that the plasma Gal3 levels of HD patients and mice correlated with disease severity. Moreover, brain Gal3 levels were higher in patients and mice with HD than those in controls. The up-regulation of Gal3 in HD mice occurred before motor impairment, and its level remained high in microglia throughout disease progression. The cell-autonomous up-regulated Gal3 formed puncta in damaged lysosomes and contributed to inflammation through NFκB- and NLRP3 inflammasome-dependent pathways. Knockdown of Gal3 suppresse","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Aug","modification":"2025-04-19T19:48:55.143Z","creation":"2019-08-09T07:04:48Z"},"accession":"S-EPMC6677843","cross_references":{"pubmed":["31375685"],"doi":["10.1038/s41467-019-11441-0"]}}