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Soft Matter. 2018 Nov 28;14(46):9466-9474. doi: 10.1039/c8sm01633j.

Molecular rotors report on changes in live cell plasma membrane microviscosity upon interaction with beta-amyloid aggregates.

Author information

1
Department of Chemistry, Imperial College London, Exhibition Road, London SW7 2AZ, UK. m.kuimova@imperial.ac.uk.

Abstract

Amyloid deposits of aggregated beta-amyloid Aβ(1-42) peptides are a pathological hallmark of Alzheimer's disease. Aβ(1-42) aggregates are known to induce biophysical alterations in cells, including disruption of plasma membranes. We investigated the microviscosity of plasma membranes upon interaction with oligomeric and fibrillar forms of Aβ(1-42). Viscosity-sensing fluorophores termed molecular rotors were utilised to directly measure the microviscosities of giant plasma membrane vesicles (GPMVs) and plasma membranes of live SH-SY5Y and HeLa cells. The fluorescence lifetimes of membrane-inserting BODIPY-based molecular rotors revealed a decrease in bilayer microviscosity upon incubation with Aβ(1-42) oligomers, while fibrillar Aβ(1-42) did not significantly affect the microviscosity of the bilayer. In addition, we demonstrate that the neuroprotective peptide H3 counteracts the microviscosity change induced by Aβ(1-42) oligomers, suggesting the utility of H3 as a neuroprotective therapeutic agent in neurodegenerative disorders and indicating that ligand-induced membrane stabilisation may be a possible mechanism of neuroprotection during neurodegenerative disorders such as Alzheimer's disease.

PMID:
30427370
DOI:
10.1039/c8sm01633j
[Indexed for MEDLINE]

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