Super-resolution imaging reveals α-synuclein seeded aggregation in SH-SY5Y cells.


Journal

Communications biology
ISSN: 2399-3642
Titre abrégé: Commun Biol
Pays: England
ID NLM: 101719179

Informations de publication

Date de publication:
21 05 2021
Historique:
received: 19 12 2020
accepted: 20 04 2021
entrez: 22 5 2021
pubmed: 23 5 2021
medline: 10 8 2021
Statut: epublish

Résumé

Aggregation of α-synuclein (α-syn) is closely linked to Parkinson's disease (PD) and the related synucleinopathies. Aggregates spread through the brain during the progression of PD, but the mechanism by which this occurs is still not known. One possibility is a self-propagating, templated-seeding mechanism, but this cannot be established without quantitative information about the efficiencies and rates of the key steps in the cellular process. To address this issue, we imaged the uptake and seeding of unlabeled exogenous α-syn fibrils by SH-SY5Y cells and the resulting secreted aggregates, using super-resolution microscopy. Externally-applied fibrils very inefficiently induced self-assembly of endogenous α-syn in a process accelerated by the proteasome. Seeding resulted in the increased secretion of nanoscopic aggregates (mean 35 nm diameter), of both α-syn and Aβ. Our results suggest that cells respond to seed-induced disruption of protein homeostasis predominantly by secreting nanoscopic aggregates; this mechanism may therefore be an important protective response by cells to protein aggregation.

Identifiants

pubmed: 34021258
doi: 10.1038/s42003-021-02126-w
pii: 10.1038/s42003-021-02126-w
pmc: PMC8139990
doi:

Substances chimiques

Amyloid 0
Protein Aggregates 0
SNCA protein, human 0
alpha-Synuclein 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

613

Subventions

Organisme : Parkinson's UK
ID : G-1703
Pays : United Kingdom
Organisme : Medical Research Council
Pays : United Kingdom

Références

Spillantini, M. G. & Goedert, M. Neurodegeneration and the ordered assembly of α-synuclein. Cell Tissue Res. 373, 137–148 (2018).
pubmed: 29119326 doi: 10.1007/s00441-017-2706-9
Jakes, R., Spillantini, M. G. & Goedert, M. Identification of two distinct synucleins from human brain. FEBS Lett. 345, 27–32 (1994).
pubmed: 8194594 doi: 10.1016/0014-5793(94)00395-5
Henderson, M. X., Trojanowski, J. Q. & Lee, V. M.-Y. α-Synuclein pathology in Parkinson’s disease and related α-synucleinopathies. Neurosci. Lett. 709, 134316 (2019).
pubmed: 31170426 pmcid: 7014913 doi: 10.1016/j.neulet.2019.134316
Jucker, M. & Walker, L. C. Propagation and spread of pathogenic protein assemblies in neurodegenerative diseases. Nat. Neurosci. 21, 1341–1349 (2018).
pubmed: 30258241 pmcid: 6375686 doi: 10.1038/s41593-018-0238-6
Goedert, M. Alzheimer’s and Parkinson’s diseases: the prion concept in relation to assembled Aβ, tau, and α-synuclein. Science 349, 1255555 (2015).
pubmed: 26250687 doi: 10.1126/science.1255555
Ingelsson, M. Alpha-synuclein oligomers—neurotoxic molecules in Parkinson’s disease and other lewy body disorders. Front. Neurosci. 10, 1–10 (2016).
doi: 10.3389/fnins.2016.00408
Bengoa-Vergniory, N., Roberts, R. F., Wade-Martins, R. & Alegre-Abarrategui, J. Alpha-synuclein oligomers: a new hope. Acta Neuropathol. 134, 819–838 (2017).
pubmed: 28803412 pmcid: 5663814 doi: 10.1007/s00401-017-1755-1
Luk, K. C. et al. Pathological-synuclein transmission initiates Parkinson-like neurodegeneration in nontransgenic mice. Science 338, 949–953 (2012).
pubmed: 23161999 pmcid: 3552321 doi: 10.1126/science.1227157
Danzer, K. M., Krebs, S. K., Wolff, M., Birk, G. & Hengerer, B. Seeding induced by α-synuclein oligomers provides evidence for spreading of α-synuclein pathology. J. Neurochem. 111, 192–203 (2009).
pubmed: 19686384 doi: 10.1111/j.1471-4159.2009.06324.x
Rey, N. L., Petit, G. H., Bousset, L., Melki, R. & Brundin, P. Transfer of human α-synuclein from the olfactory bulb to interconnected brain regions in mice. Acta Neuropathol. 126, 555–573 (2013).
pubmed: 23925565 pmcid: 3789892 doi: 10.1007/s00401-013-1160-3
Sang, J. C. et al. Direct observation of murine prion protein replication in vitro. J. Am. Chem. Soc. 140, 14789–14798 (2018).
pubmed: 30351023 pmcid: 6225343 doi: 10.1021/jacs.8b08311
Iljina, M. et al. Kinetic model of the aggregation of alpha-synuclein provides insights into prion-like spreading. Proc. Natl Acad. Sci. USA 113, E1206–E1215 (2016).
pubmed: 26884195 pmcid: 4780632 doi: 10.1073/pnas.1524128113
Rott, R. et al. Synuclein fate is determined by USP9X-regulated monoubiquitination. Proc. Natl Acad. Sci. USA 108, 18666–18671 (2011).
pubmed: 22065755 pmcid: 3219120 doi: 10.1073/pnas.1105725108
Rubinsztein, D. C. The roles of intracellular protein-degradation pathways in neurodegeneration. Nature 443, 780–786 (2006).
pubmed: 17051204 doi: 10.1038/nature05291
Lindersson, E. et al. Proteasomal inhibition by α-synuclein filaments and oligomers. J. Biol. Chem. 279, 12924–12934 (2004).
pubmed: 14711827 doi: 10.1074/jbc.M306390200
Winslow, A. R. et al. α-Synuclein impairs macroautophagy: implications for Parkinson’s disease. J. Cell Biol. 190, 1023–1037 (2010).
pubmed: 20855506 pmcid: 3101586 doi: 10.1083/jcb.201003122
Malkus, K. A. & Ischiropoulos, H. Regional deficiencies in chaperone-mediated autophagy underlie α-synuclein aggregation and neurodegeneration. Neurobiol. Dis. 46, 732–744 (2012).
pubmed: 22426402 pmcid: 3352979 doi: 10.1016/j.nbd.2012.03.017
Lehtonen, Š., Sonninen, T.-M., Wojciechowski, S., Goldsteins, G. & Koistinaho, J. Dysfunction of cellular proteostasis in Parkinson’s disease. Front. Neurosci. 13, 1–19 (2019).
doi: 10.3389/fnins.2019.00457
Kristiansen, M. et al. Disease-associated prion protein oligomers inhibit the 26S proteasome. Mol. Cell 26, 175–188 (2007).
pubmed: 17466621 doi: 10.1016/j.molcel.2007.04.001
Tseng, B. P., Green, K. N., Chan, J. L., Blurton-Jones, M. & LaFerla, F. M. Abeta inhibits the proteasome and enhances amyloid and tau accumulation. Neurobiol. Aging 29, 1607–1618 (2008).
pubmed: 17544172 doi: 10.1016/j.neurobiolaging.2007.04.014
Myeku, N. et al. Tau-driven 26S proteasome impairment and cognitive dysfunction can be prevented early in disease by activating cAMP-PKA signaling. Nat. Med. 22, 46–53 (2016).
pubmed: 26692334 doi: 10.1038/nm.4011
Cliffe, R. et al. Filamentous aggregates are fragmented by the proteasome holoenzyme. Cell Rep. 26, 2140–2149 (2019).
pubmed: 30784595 pmcid: 6381791 doi: 10.1016/j.celrep.2019.01.096
Li, J.-Y. et al. Lewy bodies in grafted neurons in subjects with Parkinson’s disease suggest host-to-graft disease propagation. Nat. Med. 14, 501–503 (2008).
pubmed: 18391963 doi: 10.1038/nm1746
Hansen, C. et al. α-Synuclein propagates from mouse brain to grafted dopaminergic neurons and seeds aggregation in cultured human cells. J. Clin. Invest. 121, 715–725 (2011).
pubmed: 21245577 pmcid: 3026723 doi: 10.1172/JCI43366
Reyes, J. F. et al. A cell culture model for monitoring α-synuclein cell-to-cell transfer. Neurobiol. Dis. 77, 266–275 (2015).
pubmed: 25046995 doi: 10.1016/j.nbd.2014.07.003
Bae, E.-J. et al. Lipid peroxidation product 4-hydroxy-2-nonenal promotes seeding-capable oligomer formation and cell-to-cell transfer of α-Synuclein. Antioxid. Redox Signal. 18, 770–783 (2013).
pubmed: 22867050 pmcid: 3555112 doi: 10.1089/ars.2011.4429
Lee, H.-J. et al. Dopamine promotes formation and secretion of non-fibrillar alpha-synuclein oligomers. Exp. Mol. Med. 43, 216 (2011).
pubmed: 21415592 pmcid: 3085740 doi: 10.3858/emm.2011.43.4.026
Danzer, K. M. et al. Exosomal cell-to-cell transmission of alpha synuclein oligomers. Mol. Neurodegener. 7, 42 (2012).
pubmed: 22920859 pmcid: 3483256 doi: 10.1186/1750-1326-7-42
Bae, E.-J. et al. Antibody-aided clearance of extracellular-synuclein prevents cell-to-cell aggregate transmission. J. Neurosci. 32, 13454–13469 (2012).
pubmed: 23015436 pmcid: 3752153 doi: 10.1523/JNEUROSCI.1292-12.2012
Meisl, G., Knowles, T. P. & Klenerman, D. The molecular processes underpinning prion-like spreading and seed amplification in protein aggregation. Curr. Opin. Neurobiol. 61, 58–64 (2020).
pubmed: 32092527 doi: 10.1016/j.conb.2020.01.010
Whiten, D. R. et al. Nanoscopic characterisation of individual endogenous protein aggregates in human neuronal cells. Chembiochem 19, 2033–2038 (2018).
pubmed: 30051958 pmcid: 6220870 doi: 10.1002/cbic.201800209
Eric-Kobayashi. Eric-Kobayashi/SR_toolkit: SR_toolkit for super-resolution image analysis. https://doi.org/10.5281/ZENODO.4651484 (2021).
Kumar, S. T. et al. How specific are the conformation-specific α-synuclein antibodies? Characterization and validation of 16 α-synuclein conformation-specific antibodies using well-characterized preparations of α-synuclein monomers, fibrils and oligomers with distinct struct. Neurobiol. Dis. 146, 105086 (2020).
pubmed: 32971232 doi: 10.1016/j.nbd.2020.105086
Wang, D. et al. Proteasome inhibition boosts autophagic degradation of ubiquitinated-AGR2 and enhances the antitumor efficiency of bevacizumab. Oncogene 38, 3458–3474 (2019).
pubmed: 30647455 pmcid: 6756021 doi: 10.1038/s41388-019-0675-z
Li, C. et al. Proteasome inhibition activates autophagy-lysosome pathway associated with TFEB dephosphorylation and nuclear translocation. Front. Cell Dev. Biol. 7, 1–8 (2019).
doi: 10.3389/fcell.2019.00170
Shacka, J. J., Klocke, B. J. & Roth, K. A. Autophagy, bafilomycin and cell death: the “A-B-Cs” of plecomacrolide-induced neuroprotection. Autophagy 2, 228–230 (2006).
pubmed: 16874105 doi: 10.4161/auto.2703
Wu, Y.-T. et al. Dual role of 3-methyladenine in modulation of autophagy via different temporal patterns of inhibition on class I and III phosphoinositide 3-kinase. J. Biol. Chem. 285, 10850–10861 (2010).
pubmed: 20123989 pmcid: 2856291 doi: 10.1074/jbc.M109.080796
Gustafsson, G. et al. Secretion and uptake of α-synuclein via extracellular vesicles in cultured cells. Cell. Mol. Neurobiol. 38, 1539–1550 (2018).
pubmed: 30288631 pmcid: 6223723 doi: 10.1007/s10571-018-0622-5
Hong, D., Fink, A. L. & Uversky, V. N. Structural characteristics of α-synuclein oligomers stabilized by the flavonoid baicalein. J. Mol. Biol. 383, 214–223 (2008).
pubmed: 18775438 pmcid: 2573395 doi: 10.1016/j.jmb.2008.08.039
Zijlstra, N., Blum, C., Segers-Nolten, I. M. J., Claessens, M. M. A. E. & Subramaniam, V. Molecular composition of sub-stoichiometrically labeled α-synuclein oligomers determined by single-molecule photobleaching. Angew. Chem. Int. Ed. 51, 8821–8824 (2012).
doi: 10.1002/anie.201200813
Lee, E.-J. et al. α-Synuclein activates microglia by inducing the expressions of matrix metalloproteinases and the subsequent activation of protease-activated receptor-1. J. Immunol. 185, 615–623 (2010).
pubmed: 20511551 doi: 10.4049/jimmunol.0903480
Galvagnion, C. et al. Lipid vesicles trigger α-synuclein aggregation by stimulating primary nucleation. Nat. Chem. Biol. 11, 229–234 (2015).
pubmed: 25643172 pmcid: 5019199 doi: 10.1038/nchembio.1750
Hijaz, B. A. & Volpicelli-Daley, L. A. Initiation and propagation of α-synuclein aggregation in the nervous system. Mol. Neurodegener. 15, 19 (2020).
pubmed: 32143659 doi: 10.1186/s13024-020-00368-6
Luk, K. C. et al. Exogenous α-synuclein fibrils seed the formation of Lewy body-like intracellular inclusions in cultured cells. Proc. Natl Acad. Sci. USA 106, 20051–20056 (2009).
pubmed: 19892735 pmcid: 2785290 doi: 10.1073/pnas.0908005106
Karpowicz, R. J. et al. Selective imaging of internalized proteopathic α-synuclein seeds in primary neurons reveals mechanistic insight into transmission of synucleinopathies. J. Biol. Chem. 292, 13482–13497 (2017).
pubmed: 28611062 pmcid: 5555207 doi: 10.1074/jbc.M117.780296
Apetri, M. M. et al. Direct observation of α-synuclein amyloid aggregates in endocytic vesicles of neuroblastoma cells. PLoS ONE 11, e0153020 (2016).
pubmed: 27105068 pmcid: 4841506 doi: 10.1371/journal.pone.0153020
Domert, J. et al. Aggregated alpha-synuclein transfer efficiently between cultured human neuron-like cells and localize to lysosomes. PLoS ONE 11, e0168700 (2016).
pubmed: 28030591 pmcid: 5193351 doi: 10.1371/journal.pone.0168700
Goold, R. et al. Rapid cell-surface prion protein conversion revealed using a novel cell system. Nat. Commun. 2, 281 (2011).
pubmed: 21505437 doi: 10.1038/ncomms1282
Gribaudo, S. et al. Propagation of α-synuclein strains within human reconstructed neuronal network. Stem Cell Rep. 12, 230–244 (2019).
doi: 10.1016/j.stemcr.2018.12.007
Pinotsi, D. et al. Nanoscopic insights into seeding mechanisms and toxicity of α-synuclein species in neurons. Proc. Natl Acad. Sci. USA 113, 3815–3819 (2016).
pubmed: 26993805 pmcid: 4833232 doi: 10.1073/pnas.1516546113
Brahic, M., Bousset, L., Bieri, G., Melki, R. & Gitler, A. D. Axonal transport and secretion of fibrillar forms of α-synuclein, Aβ42 peptide and HTTExon 1. Acta Neuropathol. 131, 539–548 (2016).
pubmed: 26820848 pmcid: 4789229 doi: 10.1007/s00401-016-1538-0
Stuendl, A. et al. Induction of α-synuclein aggregate formation by CSF exosomes from patients with Parkinson’s disease and dementia with Lewy bodies. Brain 139, 481–494 (2016).
pubmed: 26647156 doi: 10.1093/brain/awv346
Morgan, S. A. et al. α-Synuclein filaments from transgenic mouse and human synucleinopathy-containing brains are major seed-competent species. J. Biol. Chem. 295, 6652–6664 (2020).
pubmed: 32209651 pmcid: 7212628 doi: 10.1074/jbc.RA119.012179
Hughes, C. D. et al. Picomolar concentrations of oligomeric alpha-synuclein sensitizes TLR4 to play an initiating role in Parkinson’s disease pathogenesis. Acta Neuropathol. 137, 103–120 (2019).
pubmed: 30225556 doi: 10.1007/s00401-018-1907-y
Hoyer, W. et al. Dependence of α-Synuclein aggregate morphology on solution conditions. J. Mol. Biol. 322, 383–393 (2002).
pubmed: 12217698 doi: 10.1016/S0022-2836(02)00775-1
Jungmann, R. et al. Multiplexed 3D cellular super-resolution imaging with DNA-PAINT and Exchange-PAINT. Nat. Methods 11, 313–318 (2014).
pubmed: 24487583 pmcid: 4153392 doi: 10.1038/nmeth.2835
Edelstein, A. D. et al. Advanced methods of microscope control using μManager software. J. Biol. Methods 1, 10 (2014).
doi: 10.14440/jbm.2014.36
vonDiezmann, A., Shechtman, Y. & Moerner, W. E. Three-dimensional localization of single molecules for super-resolution imaging and single-particle tracking. Chem. Rev. 117, 7244–7275 (2017).
doi: 10.1021/acs.chemrev.6b00629
Schindelin, J. et al. Fiji: an open-source platform for biological-image analysis. Nat. Methods 9, 676–682 (2012).
pubmed: 22743772 doi: 10.1038/nmeth.2019
Fröhlich, E. et al. Comparison of two in vitro systems to assess cellular effects of nanoparticles-containing aerosols. Toxicol. Vitr. 27, 409–417 (2013).
doi: 10.1016/j.tiv.2012.08.008
Courte, J. et al. The expression level of alpha-synuclein in different neuronal populations is the primary determinant of its prion-like seeding. Sci. Rep. 10, 4895 (2020).
pubmed: 32184415 pmcid: 7078319 doi: 10.1038/s41598-020-61757-x

Auteurs

Jason C Sang (JC)

Department of Chemistry, University of Cambridge, Cambridge, UK.
UK Dementia Research Institute at Cambridge, Cambridge, UK.

Eric Hidari (E)

Department of Chemistry, University of Cambridge, Cambridge, UK.
UK Dementia Research Institute at Cambridge, Cambridge, UK.

Georg Meisl (G)

Department of Chemistry, University of Cambridge, Cambridge, UK.

Rohan T Ranasinghe (RT)

Department of Chemistry, University of Cambridge, Cambridge, UK.

Maria Grazia Spillantini (MG)

Department of Clinical Neuroscience, University of Cambridge, Cambridge, UK.

David Klenerman (D)

Department of Chemistry, University of Cambridge, Cambridge, UK. dk10012@cam.ac.uk.
UK Dementia Research Institute at Cambridge, Cambridge, UK. dk10012@cam.ac.uk.

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