ANISOTROPIC STRAIN EFFECTS ON VASCULAR SMOOTH MUSCLE CELL PHYSIOLOGY

摘要

Biological development is a complex and highly-regulated process, a significant part of which is controlled by mechanostimulus, or the strain imparted on a cell by its environment. Mechanostimulus is important for stem cell differentiation, from cytoskeletal assembly to cell-cell and cell-matrix adhesion [1]. The mechanics of cells and tissues play a critical role in organisms, under both physiological and pathological conditions; abnormal mechanotransduction - the mechanism by which cells sense and respond to strain - has been implicated in a wide range of clinical pathologies [2,3]. Strain as a developmental regulator is especially pertinent for vascular smooth muscle cells (SMCs), as they exist in an environment of cyclic mechanical strain imposed on the vasculature by the heart pumping blood through it. SMC phenotype ultimately depends on an interplay of myriad factors, and strain conditions have been connected to genetic upregulation and downregulation, proliferation, apoptosis, and organization of intracellular structures as well as cells into tissues. Physiological data shows that in vivo, vascular SMCs experience anisotropic biaxial strain. Understanding anisotropic strain requires some understanding of cell morphology. The functionality of a smooth muscle cell resides in its contractile unit, the myofibril - an interlaced network of parallel actin and myosin filaments that slide over each other to induce contraction. An SMC has a major and a minor axis. The major axis runs parallel to the myofibril, while the minor axis runs perpendicular to the myofibril; thus, the cell always contracts along its major axis. The axes determine the strain type: anisotropic biaxial strain propagates in different magnitudes across each axis of the cell (Figure 1). In this study, we present the effects of anisotropic biaxial strain on vascular SMC viability, functionality, and proliferation.