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Abstract
Vascular endothelial cells are subjected to hemodynamic forces such as mechanical stretch due to the pulsatile nature of blood flow. Mechanical stretch of different intensities is detected by mechanoreceptors on the cell surface which enables the conversion of external mechanical stimuli to biochemical signals in the cell, activating downstream signaling pathways. This activation may vary depending on whether the cell is exposed to physiological or pathological stretch intensities. Substantial stretch associated with normal physiological functioning is important in maintaining vascular homeostasis as it is involved in the regulation of cell structure, vascular angiogenesis, proliferation and control of vascular tone. However, the elevated pressure that occurs with hypertension exposes cells to excessive mechanical load, and this may lead to pathological consequences through the formation of reactive oxygen species, inflammation and/or apoptosis. These processes are activated by downstream signaling through various pathways that determine the fate of cells. Identification of the proteins involved in these processes may help elucidate novel mechanisms involved in vascular disease associated with pathological mechanical stretch and could provide new insight into therapeutic strategies aimed at countering the mechanisms’ negative effects.
Highlights
Blood vessels consist of three primary layers: the tunica intima, the tunica media and the tunica adventitia
The tunica intima is the innermost layer that contains the endothelium (endothelial cell (EC) layers) that provides a smooth surface for blood flow, whereas the tunica media contains thick layers of elastin, collagen and smooth muscle cells (SMCs) for vascular dilation or constriction
There will be a particular emphasis on receptors involved in sensing mechanical stretch; the signal transduction pathways involved that result in extracellular matrix (ECM) remodeling, angiogenesis, cell proliferation, vascular tone homeostasis, reactive oxygen species formation, inflammation and apoptosis (Table 1)
Summary
Blood vessels consist of three primary layers: the tunica intima, the tunica media and the tunica adventitia. The outermost layer, the tunica adventitia, is composed of a mixture of connective tissue, collagen and elastic fibers and is used for arterial support Hemodynamic forces, such as shear and tensile stress, continuously act upon blood vessels due to the pumping motion of the heart. The effect of tensile stretch ( on human vascular ECs), has not been studied in depth [ 9– 12] For this reason, this review will focus on the current research in mechanotransduction as it relates to vascular ECs. There will be a particular emphasis on receptors involved in sensing mechanical stretch; the signal transduction pathways involved that result in extracellular matrix (ECM) remodeling, angiogenesis, cell proliferation, vascular tone homeostasis, reactive oxygen species formation, inflammation and apoptosis (Table 1). Paxillin needed for initial cell orientation Rho proteins for perpendicular alignment
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