Flow Stimulates ICAM-1 Expression Time and Shear Stress Dependently in Cultured Human Endothelial Cells

Shear stress induces expression of CNP gene in human endothelial cells

“…However, endothelial cells are known to have mechanoreceptors by which changes in blood flow or shear stress are recognized by the endothelial cell and the signal is transmitted to intracellular organelles [17]. Recently, several studies clarified that shear stress exerts an influence on the expression of mRNA such as tissue plasminogen activator, ICAM-1, TGF-fll and constitutive nitric oxide synthase (cNOS) mRNA [10][11][12]18]. Promoter analysis of these substance revealed a specific base arrangement; 'GAGACC' or 'GGTCTC', shear stress responsive element (SSRE), exists in the promoter region of these gene [19].…”

Primary Prevention of Ischemic Stroke

“…Shear stress and turbulence may contribute to adhesion receptor expression and may explain the localization of atherosclerotic plaques at vessel bifurcations. [252][253][254] Monocytes and T cells bind to the expressed adhesion molecules, become activated, and secrete products such as cytokines and proteolytic enzymes that contribute to vessel damage. Markers of inflammation, such as leukocyte adhesion receptors 255 and cytokines, 256 as well as activated T cells and macrophages, 257 are present in carotid endarterectomy specimens of recently symptomatic patients, which suggests that acute inflammatory responses may predispose to plaque destabilization and symptoms.…”

Fluid Shear Stress Transcriptionally Induces Lectin-like Oxidized LDL Receptor-1 in Vascular Endothelial Cells

“…1,2 Fluid shear stress has been shown to modulate a variety of endothelial functions, including the expression of a variety of genes, such as endothelin-1, [3][4][5] cyclooxygenase-2, 6 NO synthase, 6,7 tissue factor, 8 transforming growth factor-␤, 9 platelet-derived growth factor (PDGF), 10,11 basic fibroblast growth factor, 11 heparin-binding epidermal growth factor-like growth factor, 12 monocyte chemotactic protein-1, 13 intercellular adhesion molecule-1, 14,15 and vascular cell adhesion molecule-1, 16,17 as well as its effects on cytoskeletal organization and cell morphology. 4,18,19 These biological effects elicited by fluid shear stress appear to be mediated by intracellular signal transduction cascades, including intracellular Ca 2ϩ mobilization, 20 -22 inositol trisphosphate, 23 K ϩ channel, 24 G protein, 25 mitogen-activated protein kinases, 26,27 N-terminal Jun kinase, 28,29 and platelet endothelial cell adhesion molecule-1 tyrosine phosphorylation, 30 and by the subsequent activation of transcription factors, such as activator protein-1 (AP-1), 31,32 nuclear factor-B (NF-B), 31,33 and Egr-1 (an early growth response gene product), 34,35 and may potentially affect vascular tone, thrombus formation, and atherogenesis.…”