Abstract
The process of clustering of plasma membrane receptors in response to their agonist is the first step in signal transduction. The rate of the clustering process and the size of the clusters determine further cell responses. Here we aim to demonstrate that a simple 2-differential equation mathematical model is capable of quantitative description of the kinetics of 2D or 3D cluster formation in various processes. Three mathematical models based on mass action kinetics were considered and compared with each other by their ability to describe experimental data on GPVI or CR3 receptor clustering (2D) and albumin or platelet aggregation (3D) in response to activation. The models were able to successfully describe experimental data without losing accuracy after switching between complex and simple models. However, additional restrictions on parameter values are required to match a single set of parameters for the given experimental data. The extended clustering model captured several properties of the kinetics of cluster formation, such as the existence of only three typical steady states for this system: unclustered receptors, receptor dimers, and clusters. Therefore, a simple kinetic mass-action-law-based model could be utilized to adequately describe clustering in response to activation both in 2D and in 3D.
Highlights
The process of clustering of the receptors during cell activation is a crucial step for correct cell response in a plethora of signaling pathways [1,2,3]
We performed an investigation of the impact of model parameters on its behavior and/or compared the ability to describe the experimental data between the full model and the “2-equation model”
Since aggregation is considered to be the most general case of coagulation and fragmentation, we started with the investigation of the “Aggregation model” and “2-equation model” models for the aggregation process and used the data of bovine serum albumin (BSA) aggregation
Summary
The process of clustering of the receptors during cell activation is a crucial step for correct cell response in a plethora of signaling pathways [1,2,3]. Life 2020, 10, 97 the amplification of the initial signal [6,7,8,9] by either an enhancement of the affinity of the receptors for the ligand [10,11,12,13] or the intracellular signaling proteins [14] or by other mechanisms [15,16,17]. The underlying mechanisms of the receptor clustering resemble particle aggregation or protein polymerization. A mathematical model of particle aggregation could be applied to receptor clustering or protein polymerization upon simplification and imposition of the dimensional restrictions
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