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Title:Cyanobacterial cyclic peptides can disrupt cytoskeleton organization in human astrocytes : a contribution to the understanding of the systemic toxicity of cyanotoxins
Authors:ID Bubik, Anja (Author)
ID Frangež, Robert (Author)
ID Žužek, Monika C. (Author)
ID Gutiérrez-Aguirre, Ion (Author)
ID Lah Turnšek, Tamara (Author)
ID Sedmak, Bojan (Author)
Files:URL URL - Source URL, visit https://doi.org/10.3390/toxins16090374
 
.pdf PDF - Presentation file, download (21,09 MB)
MD5: E7C76924AF8B510314F095D2393A909B
 
Language:English
Typology:1.01 - Original Scientific Article
Organization:Logo NIB - National Institute of Biology
Abstract:The systemic toxicity of cyclic peptides produced by cyanobacteria (CCPs) is not yet completely understood. Apart from the most known damages to the liver and kidneys, symptoms of their neurotoxicity have also been reported. Hepatotoxic CCPs, like microcystins, as well as non-hepatotoxic anabaenopeptins and planktopeptins, all exhibit cytotoxic and cytostatic effects on mammalian cells. However, responses of different cell types to CCPs depend on their specific modes of interaction with cell membranes. This study demonstrates that non-hepatotoxic planktopeptin BL1125 and anabaenopeptins B and F, at concentrations up to 10 µM, affect normal and tumor human astrocytes (NHA and U87-GM) in vitro by their almost immediate insertion into the lipid monolayer. Like microcystin-LR (up to 1 µM), they inhibit Ser/Thr phosphatases and reorganize cytoskeletal elements, with modest effects on their gene expression. Based on the observed effects on intermediate filaments and intermediate filament linkage elements, their direct or indirect influence on tubulin cytoskeletons via post-translational modifications, we conclude that the basic mechanism of CCP toxicities is the induction of inter- and intracellular communication failure. The assessed inhibitory activity on Ser/Thr phosphatases is also crucial since the signal transduction cascades are modulated by phosphorylation/dephosphorylation processes.
Keywords:astrocytes, cyclic cyanobacterial peptides, cytoskeletal organization, Ser/Thr phosphatases, systemic toxicity, cyanobacteria
Publication status:Published
Publication version:Version of Record
Publication date:01.09.2024
Year of publishing:2024
Number of pages:str. 1-18
Numbering:iss. 9, [art no.] ǂ374
PID:20.500.12556/DiRROS-20241 New window
UDC:576
ISSN on article:2072-6651
DOI:10.3390/toxins16090374 New window
COBISS.SI-ID:205590019 New window
Note:Soavtorji: Robert Frangež, Monika C. Žužek, Ion Gutiérrez-Aguirre, Tamara T. Lah and Bojan Sedmak; Nasl. z nasl. zaslona; Opis vira z dne 28. 8. 2024;
Publication date in DiRROS:28.08.2024
Views:11
Downloads:5
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Record is a part of a journal

Title:Toxins : Elektronski vir
Shortened title:Toxins
Publisher:MDPI
ISSN:2072-6651
COBISS.SI-ID:517594649 New window

Document is financed by a project

Funder:ARIS - Slovenian Research and Innovation Agency
Project number:J1-0848-2008
Name:Antikancerogeno delovanje bioaktivnih spojin cianobakterijskega izvora v nasprotju možganskih tumorjev - gliobastomov

Funder:ARIS - Slovenian Research and Innovation Agency
Project number:P4-0053-2019
Name:Endokrini, imunski in encimski odzivi pri zdravih in bolnih živalih

Funder:Other - Other funder or multiple funders
Funding programme:Ministry of Defense, Administration for Civil Protection and Disaster Relief
Project number:URSZR 4300-1117/2009-1

Licences

License:CC BY 4.0, Creative Commons Attribution 4.0 International
Link:http://creativecommons.org/licenses/by/4.0/
Description:This is the standard Creative Commons license that gives others maximum freedom to do what they want with the work as long as they credit the author.

Secondary language

Language:Slovenian
Title:Cyanobacterial cyclic peptides can disrupt cytoskeleton organization in human astrocytes – a contribution to the understanding of the systemic toxicity of cyanotoxins
Keywords:astrociti, ciklični cianobakterijski peptidi, citoskeletna organizacija, Ser/Thr fosfataze, sistemska toksičnost, cianobakterije


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