Maleš Petra, Pem Barbara, Petrov Dražen, Mangiarotti Agustín, Dimova Rumiana, Bakarić Danijela
Division of Organic Chemistry and Biochemistry, Ruđer Bošković Institute, Bijenička 54, 10000 Zagreb, Croatia.
Institute of Molecular Modeling and Simulation, University of Natural Resources and Life Sciences, 1180 Vienna, Austria.
Membranes (Basel). 2025 Sep 17;15(9):279. doi: 10.3390/membranes15090279.
Myelin is a lipid-rich membrane that insulates axons, providing support and ensuring efficient nerve impulse conduction. Disruption of this sheath, or demyelination, impairs neural transmission and underlies symptoms like vision loss and muscle weakness in multiple sclerosis (MS). Despite extensive studies using in vitro and in vivo models, the molecular mechanisms driving demyelination remain incompletely understood. To investigate the role of myelin basic protein (MBP) in membrane stability, we prepared model myelin membranes (MMMs) from lipids expectedly undergoing gel-to-fluid phase transition, mimicking both normal and altered myelin, with and without MBP. Differential scanning calorimetry (DSC) revealed that MBP suppresses the main phase transition in normal MMMs, unlike in modified MMMs. FTIR spectra showed strengthening of van der Waals interactions in normal MMMs with MBP upon heating and opposite effects in the analogous modified MMM system. Additionally, phosphate groups were identified as critical sites for MBP-lipid interactions. Circular dichroism (CD) spectroscopy suggests that MBP adopts helical structures that penetrate the bilayer of normal MMMs. These findings offer new insights into the molecular-level interactions between MBP and myelin membranes, with implications for understanding demyelination in diseases like MS.