{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["12"],"submitter":["Limanaqi F"],"pubmed_abstract":["<b>Introduction:</b> Abnormal spreading of alpha-synuclein (αS), a hallmark of Parkinson's disease, is known to promote peripheral inflammation, which occurs in part via functional alterations in monocytes/macrophages. However, underlying intracellular mechanisms remain unclear. <b>Methods:</b> Herein we investigate the subcellular, molecular, and functional effects of excess αS in human THP-1 monocytic cell line, THP-1-derived macrophages, and at least preliminarily, in primary monocyte-derived macrophages (MDMs). In cells cultured w/wo recombinant αS (1 μM) for 4 h and 24 h, by Confocal microscopy, Western Blot, RT-qPCR, Elisa, and Flow Cytometry we assessed: i) αS internalization; ii) cytokine/chemokine expression/secretion, and C-C motif chemokine receptor 2 (CCR2) levels; iii) autopha"],"journal":["Frontiers in cell and developmental biology"],"pagination":["1421360"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11257978"],"repository":["biostudies-literature"],"pubmed_title":["Alpha-synuclein shapes monocyte and macrophage cell biology and functions by bridging alterations of autophagy and inflammatory pathways."],"pmcid":["PMC11257978"],"pubmed_authors":["Trabattoni D","Ogno P","Fenizia C","Vanetti C","Zecchini S","Garziano M","Clerici M","Biasin M","Artusa V","Limanaqi F","Saulle I","Strizzi S"],"additional_accession":[]},"is_claimable":false,"name":"Alpha-synuclein shapes monocyte and macrophage cell biology and functions by bridging alterations of autophagy and inflammatory pathways.","description":"<b>Introduction:</b> Abnormal spreading of alpha-synuclein (αS), a hallmark of Parkinson's disease, is known to promote peripheral inflammation, which occurs in part via functional alterations in monocytes/macrophages. However, underlying intracellular mechanisms remain unclear. <b>Methods:</b> Herein we investigate the subcellular, molecular, and functional effects of excess αS in human THP-1 monocytic cell line, THP-1-derived macrophages, and at least preliminarily, in primary monocyte-derived macrophages (MDMs). In cells cultured w/wo recombinant αS (1 μM) for 4 h and 24 h, by Confocal microscopy, Western Blot, RT-qPCR, Elisa, and Flow Cytometry we assessed: i) αS internalization; ii) cytokine/chemokine expression/secretion, and C-C motif chemokine receptor 2 (CCR2) levels; iii) autopha","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024","modification":"2025-04-04T14:46:39.831Z","creation":"2025-04-04T14:46:39.831Z"},"accession":"S-EPMC11257978","cross_references":{"pubmed":["39035028"],"doi":["10.3389/fcell.2024.1421360"]}}