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Sökning: onr:"swepub:oai:DiVA.org:uu-425626" > Crosstalk between a...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00005660naa a2200613 4500
001oai:DiVA.org:uu-425626
003SwePub
008201117s2021 | |||||||||||000 ||eng|
009oai:prod.swepub.kib.ki.se:146825593
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4256262 URI
0247 a https://doi.org/10.1186/s12974-021-02158-32 DOI
0247 a http://kipublications.ki.se/Default.aspx?queryparsed=id:1468255932 URI
040 a (SwePub)uud (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Rostami, Jinaru Uppsala universitet,Geriatrik4 aut0 (Swepub:uu)jinro821
2451 0a Crosstalk between astrocytes and microglia results in increased degradation of α-synuclein and amyloid-β aggregates
264 c 2021-06-03
264 1b Springer Science and Business Media LLC,c 2021
338 a electronic2 rdacarrier
500 a Title in thesis list of papers: Cross-talk between astrocytes and microglia results in increased degradation of α-synuclein and amyloid-β aggregates
520 a BackgroundAlzheimer’s disease (AD) and Parkinson’s disease (PD) are characterized by brain accumulation of aggregated amyloid-beta (Aβ) and alpha-synuclein (αSYN), respectively. In order to develop effective therapies, it is crucial to understand how the Aβ/αSYN aggregates can be cleared. Compelling data indicate that neuroinflammatory cells, including astrocytes and microglia, play a central role in the pathogenesis of AD and PD. However, how the interplay between the two cell types affects their clearing capacity and consequently the disease progression remains unclear.MethodsThe aim of the present study was to investigate in which way glial crosstalk influences αSYN and Aβ pathology, focusing on accumulation and degradation. For this purpose, human-induced pluripotent cell (hiPSC)-derived astrocytes and microglia were exposed to sonicated fibrils of αSYN or Aβ and analyzed over time. The capacity of the two cell types to clear extracellular and intracellular protein aggregates when either cultured separately or in co-culture was studied using immunocytochemistry and ELISA. Moreover, the capacity of cells to interact with and process protein aggregates was tracked using time-lapse microscopy and a customized “close-culture” chamber, in which the apical surfaces of astrocyte and microglia monocultures were separated by a <1 mm space.ResultsOur data show that intracellular deposits of αSYN and Aβ are significantly reduced in co-cultures of astrocytes and microglia, compared to monocultures of either cell type. Analysis of conditioned medium and imaging data from the “close-culture” chamber experiments indicate that astrocytes secrete a high proportion of their internalized protein aggregates, while microglia do not. Moreover, co-cultured astrocytes and microglia are in constant contact with each other via tunneling nanotubes and other membrane structures. Notably, our live cell imaging data demonstrate that microglia, when attached to the cell membrane of an astrocyte, can attract and clear intracellular protein deposits from the astrocyte.ConclusionsTaken together, our data demonstrate the importance of astrocyte and microglia interactions in Aβ/αSYN clearance, highlighting the relevance of glial cellular crosstalk in the progression of AD- and PD-related brain pathology.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Neurovetenskaper0 (SwePub)301052 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Neurosciences0 (SwePub)301052 hsv//eng
653 a Alzheimer's disease
653 a Parkinson's disease
653 a alpha-Synuclein
653 a Crosstalk
653 a Amyloid-beta
653 a Astrocyte
653 a Microglia
653 a Co-culture
653 a Degradation
653 a Tunneling nanotube
7001 a Mothes, Tobiasu Uppsala universitet,Geriatrik4 aut0 (Swepub:uu)tobmo639
7001 a Kolahdouzan, Mahshadu Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University4 aut
7001 a Eriksson, Olleu Uppsala universitet,Institutionen för medicinsk cellbiologi4 aut0 (Swepub:uu)oller336
7001 a Moslem, Mohsenu Department of Neuroscience, Karolinska Institutet4 aut
7001 a Bergström, Joakimu Uppsala universitet,Geriatrik4 aut0 (Swepub:uu)joakberg
7001 a Ingelsson, Martinu Uppsala universitet,Geriatrik4 aut0 (Swepub:uu)maing121
7001 a O'Callaghan, Paulu Uppsala universitet,Institutionen för medicinsk cellbiologi4 aut0 (Swepub:uu)pauoo824
7001 a Healy, Luke M.u Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University4 aut
7001 a Falk, Annau Karolinska Institutet4 aut
7001 a Erlandsson, Annau Uppsala universitet,Geriatrik4 aut0 (Swepub:uu)annafors
7102 a Uppsala universitetb Geriatrik4 org
7730 t Journal of Neuroinflammationd : Springer Science and Business Media LLCg 18:1q 18:1x 1742-2094
8564 u https://doi.org/10.1186/s12974-021-02158-3y Fulltext
8564 u https://uu.diva-portal.org/smash/get/diva2:1501653/FULLTEXT01.pdfx primaryx Raw objecty fulltext:print
8564 u https://jneuroinflammation.biomedcentral.com/track/pdf/10.1186/s12974-021-02158-3
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-425626
8564 8u https://doi.org/10.1186/s12974-021-02158-3
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:146825593

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