The Effect of Pressure-Induced Mechanical Stretch on Vascular Wall Differential Gene Expression

Abstract

High blood pressure is responsible for the modulation of blood vessel morphology and function. Arterial hypertension is considered to play a significant role in atherosclerotic ischaemic heart disease, stroke and hypertensive nephropathy, whereas high venous pressure causes varicose vein formation and chronic venous insufficiency and contributes to vein bypass graft failure. Hypertension exerts differing injurious forces on the vessel wall, namely shear stress and circumferential stretch. Morphological and molecular changes in blood vessels ascribed to elevated pressure consist of endothelial damage, neointima formation, activation of inflammatory cascades, hypertrophy, migration and phenotypic changes in vascular smooth muscle cells, as well as extracellular matrix imbalances. Differential expression of genes encoding relevant factors including vascular endothelial growth factor, endothelin-1, interleukin-6, vascular cell adhesion molecule, intercellular adhesion molecule, matrix metalloproteinase-2 and -9 and plasminogen activator inhibitor-1 has been explored using ex vivo cellular or organ stretch models and in vivo experimental animal models. Identification of pertinent genes may unravel new therapeutic strategies to counter the effects of pressure-induced stretch on the vessel wall and hence minimise its notable complications.

Gold nanoparticle interactions with endothelial cells cultured under physiological conditions

“…This is also in agreement with the data previously published by Fede et al who detected the same tendency for the internalization of AuNPs (w/o PEG) in HUVEC under static and flow conditions using a microfluidic system. 36 In addition to shear stress, cyclic stretch is also a prominent hemodynamic force which acts on endothelial cell function and membrane traffic 17,37 and may alter the internalization of nanoparticles in endothelial cells. As previously reported, we showed that stretch affects the interaction of endothelial cells with amorphous silica nanoparticles and leads to a reduced internalization.…”

Wall shear stress in the development of in-stent restenosis revisited. A critical review of clinical data on shear stress after intracoronary stent implantation

“…Although the mechanisms controlling the response of SMCs to mechanical stress have not been fully clarified, it seems that mechanical stretch is transmitted to the SMCs through macromolecular protein complexes, such as transmembrane integrins binding with intracellular adaptors (e.g., paxillin and vinculin) and signaling proteins (focal adhesion kinases) [36][37][38]. Macroscopically, stent placement induces straightening of arterial segments, slightly altering the distribution of shear stress.…”

Relationship between carotid artery atherosclerosis and sulfatide in hypertensive patients

“…One theory is that an elevated pulse pressure causes greater stretching of the arteries, which induces fatigue and fracture of the elastic elements and thus is likely to hasten the development of intimal damage that leads to atherosclerosis. Another theory is that elevated blood pressure promotes inflammatory activation of the arterial wall, which increases the risk of atherosclerosis (Chae et al, 2001;Amer et al, 2011;Anwar et al, 2012).…”

“…They are widely distributed in the organs and sera of various animals, including humans. Studies have demonstrated a role for sulfatides in atherogenesis and vascular inflammation resulting in atherosclerosis (Hara et al, 1996;Anwar et al, 2012). An increase in sulfatide was found in both lipoprotein and atherosclerotic plaques in the Watanabe heritable hyperlipidemic rabbit -an animal model for human familial hypercholesterolemia -and was intimately correlated with the development of atherosclerosis (Hara et al, 1996).…”