Institute of Physics, Polish Academy of Sciences, Al. Lotnikow 32/46, 02-668 Warsaw, Poland.
Institute for Computational Science and Technology, SBI Building, Quang Trung Software City, Tan Chanh Hiep Ward, District 12, Ho Chi Minh City 700000, Vietnam.
Biomolecules. 2021 Apr 18;11(4):596. doi: 10.3390/biom11040596.
The self-assembly of amyloidogenic peptides and proteins into fibrillar structures has been intensively studied for several decades, because it seems to be associated with a number of neurodegenerative diseases, such as Alzheimer's and Parkinson's disease. Therefore, understanding the molecular mechanisms of this phenomenon is important for identifying an effective therapy for the corresponding diseases. Protein aggregation in living organisms very often takes place on surfaces like membranes and the impact of a surface on this process depends not only on the surface chemistry but also on its topology. Our goal was to develop a simple lattice model for studying the role of surface roughness in the aggregation kinetics of polypeptide chains and the morphology of aggregates. We showed that, consistent with the experiment, an increase in roughness slows down the fibril formation, and this process becomes inhibited at a very highly level of roughness. We predicted a subtle catalytic effect that a slightly rough surface promotes the self-assembly of polypeptide chains but does not delay it. This effect occurs when the interaction between the surface and polypeptide chains is moderate and can be explained by taking into account the competition between energy and entropy factors.
几十年来,人们一直在深入研究淀粉样肽和蛋白质的自组装成纤维状结构,因为它似乎与许多神经退行性疾病有关,如阿尔茨海默病和帕金森病。因此,了解这一现象的分子机制对于确定相应疾病的有效治疗方法很重要。在生物体中,蛋白质聚集通常发生在膜等表面上,表面对这个过程的影响不仅取决于表面化学性质,还取决于其拓扑结构。我们的目标是开发一个简单的格子模型,用于研究表面粗糙度在多肽链聚集动力学和聚集体形态中的作用。我们表明,与实验一致,粗糙度的增加会减缓原纤维的形成,而在非常高的粗糙度水平下,这个过程会被抑制。我们预测了一个微妙的催化效应,即略微粗糙的表面会促进多肽链的自组装,但不会延迟它。当表面与多肽链之间的相互作用适中时,就会出现这种效应,这可以通过考虑能量和熵因素之间的竞争来解释。