RT Journal Article
T1 Molecular rotors report on changes in live cell plasma membrane microviscosity upon interaction with beta-amyloid aggregates
A1 López Duarte, Ismael
A1 Markéta Kubánková, 
A1 Darya Kiryushko, 
A1 Marina K. Kuimova, 
AB Amyloid deposits of aggregated beta-amyloid A(1-42) peptides are a pathological hallmark of Alzheimer's disease. A(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 A(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 A(1-42) oligomers, while fibrillar A(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 A(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.
PB Royal Society of Chemistry
SN 1744-683X
SN 1744-6848
YR 2018
FD 2018
LK https://hdl.handle.net/20.500.14352/115177
UL https://hdl.handle.net/20.500.14352/115177
LA eng
NO Kubánková M, López-Duarte I, Kiryushko D, Kuimova MK. Molecular rotors report on changes in live cell plasma membrane microviscosity upon interaction with beta-amyloid aggregates. Soft Matter 2018;14:9466–74. https://doi.org/10.1039/C8SM01633J.
DS Docta Complutense
RD 16 abr 2025