Smooth muscle cell vascular

The calcification of atherosclerotic plaques may be induced by osteopontin expression, since osteopontin is a protein with a well-characterized role in bone formation and calcification. Vascular smooth muscle cell migration on osteopontin is dq endent on the integrin av 33 and antagonists of av 33 prevent both smooth muscle cell migration and restenosis in some animal model [8]. 

In addition to intracellular heme-containing proteins, big-conductance calcium-dependent K+ (BKCa) channels and calcium-spark activated transient Kca channels in plasma membrane are also tar geted by CO [3]. As well known, nitric oxide (NO) also activates BKca channels in vascular smooth muscle cells. While both NO and CO open BKCa channels, CO mainly acts on alpha subunit of BKCa channels and NO mainly acts on beta subunit of BKca channels in vascular smooth muscle cells. Rather than a redundant machinery, CO and NO provide a coordinated regulation of BKca channel function by acting on different subunits of the same protein complex. Furthermore, pretreatment of vascular smooth muscle... 

Human umbilical vein endothelial cells (HUVEC) express the isoforms ECE-la, -lb, -Id and ECE-2. In these cells, ET-1 is secreted via both a constitutive and a regulated pathway. The ratio of released ET-1 big-ET-1 is 4 1. About 80% of the ET-1 is secreted at the abluminal cell surface of endothelial cells. ECE-isoforms are abundantly expressed on the cell surface of endothelial cells and to a lower level also on vascular smooth muscle cells. In atherosclerotic lesions of vessels, however, ECE expression in smooth muscle cells is upregulated. ECE isoforms expressed in smooth muscle cells contribute significantly to the generation of mature ET in normal and in particular atherosclerotic vessels. 

The ETa receptor activates G proteins of the Gq/n and G12/i3 family. The ETB receptor stimulates G proteins of the G and Gq/11 family. In endothelial cells, activation of the ETB receptor stimulates the release of NO and prostacyclin (PGI2) via pertussis toxin-sensitive G proteins. In smooth muscle cells, the activation of ETA receptors leads to an increase of intracellular calcium via pertussis toxin-insensitive G proteins of the Gq/11 family and to an activation of Rho proteins most likely via G proteins of the Gi2/i3 family. Increase of intracellular calcium results in a calmodulin-dependent activation of the myosin light chain kinase (MLCK, Fig. 2). MLCK phosphorylates the 20 kDa myosin light chain (MLC-20), which then stimulates actin-myosin interaction of vascular smooth muscle cells resulting in vasoconstriction. Since activated Rho... 

Sites of endothelin-receptor expression. ETA receptors are expressed in the smooth muscle cells of the vascular medial layer and the airways, in cardiac myocytes, lung parenchyma, bronchiolar epithelial cells and prostate epithelial cells. ETB receptors are expressed in endothelial cells, in bronchiolar smooth muscle cells, vascular smooth muscle cells of certain vessels (e.g. saphenous vein, internal mammary artety), in the renal proximal and distal tubule, the renal collecting duct and in the cells of the atrioventricular conducting system. 

S1P2 Ubiquitous Gj/O. Gq, G12/13 Migration, vascular development, differentiation of vascular smooth muscle cells... 

In some cell types, e.g. in vascular smooth muscle cells, NPY appears to enhance cell growth. 

Fak kinases could be modulators of some aspects of human cancels and may also contribute to the development of vascular diseases involving hyperproliferation and migration of vascular smooth muscle cells. 

Another example was done by Opitz et al. They utilized P4HB scaffolds to produce viable ovine blood vessels, and then implanted the blood vessels in the systemic circulation of sheep. Enzymatically derived vascular smooth muscle cells (vSMC) were seeded on the scaffolds both under pulsatile flow and static conditions. Mechanical properties of bioreactor-cultured blood vessels which were obtained from tissue engineering approached those of native aorta. 

Opitz F, Schenke-Layland K, Richter W, Martin DP, Degenkolbe I, Wahlers T, and Stock UA. Tissue engineering of ovine aortic blood vessel substitutes using applied shear stress and enzymatically derived vascular smooth muscle cells. Ann Biomed Eng, 2004, 32, 212-222. 

Proliferation of vascular smooth muscle cells is one of the most important features of arteriosclerosis. Vascular smooth muscle cells display a unique... 

RAO G N and berk b c (1992) Active oxygen species stimulate vascular smooth muscle cell growth and proto-oncogene expression Circulation Research 70, 593-9. 

TASINATO A D, BOISCOBOINIK D, BARTOLI G M, MARONi p and Azzi A (1995) d-a-tocopherol inhibition of vascular smooth muscle cell proliferation occurs at physiological concentrations, correlates with protein kinase C inhibition, and is independent of its ntioydd ait xo eriie% Proceedings National Academy Sciences USA 92, 12190-4. 

TSAI J-C, JAIN M, HSIEH C-M, LEE W-S, YOSHIZUMI M, PATTERSON C, PERRELLA M A, COOKE C, WANG H, HABER E, scHLEGEL R, and LEE M E (1996) Induction of apoptosis by pyrrolidinedithiocarbamate and N-acetylcysteine in vascular smooth muscle cells Journal Biological Chemistry 271, 3667-70. 

The normal arterial wall consists of the intima, media, and adventitia, as illustrated in Fig. 4—3A. The endothelium is located in the intima and consists of a layer of endothelial cells that line the lumen of the artery and form a selective barrier between the vessel wall and blood contents. The internal elastic lamina separates the intima and media, where vascular smooth muscle cells are found. The vascular adventitia comprises the artery s outer layer. Atherosclerotic lesions form in the subendothelial space between the endothelial cells and internal elastic lamina. 

Apo E, apolipoprotein E CAD, coronary artery disease FKN, fractalkine MHC, major histocompatibility complex MCP-1, monocyte chemoattractant protein 1 MMPs, matrix metalloproteinases NK, natural killer oxLDL, oxidized LDL RANTES, regulated on activation, normal T cell expressed and secreted VSMCs, vascular smooth muscle cells. 

Fig. 2. The role of MCP-1 (CCL2)/CCR2 in atherosclerosis is thought to occur through the response of endothelial cells and vascular smooth muscle cells to oxidized lipoproteins. After injury by oxidized lipoproteins, MCP-1 is released and attracts CCR2-expressing monocytes to the site of injury and activates them to secrete inflammatory mediators.

Yu X, Dluz S, Graves DT, et al. Elevated expression of monocyte chemoattractant protein 1 by vascular smooth muscle cells in hypercholesterolemic primates. Proc Natl Acad Sci U S A 1992 89(15) 6953-6957. 

Hayes IM, Jordan NJ, Towers S, et al. Human vascular smooth muscle cells express receptors for CC chemokines. Arterioscler Thromb Vase Biol 1998 18(3) 397 103. 

Wang JM, Sica A, Peri G, et al. Expression of monocyte chemotactic protein and interleukin-8 by cytokine-activated human vascular smooth muscle cells. Arterioscler Thromb 1991 11(5) 1166—1174. 

In conclusion, ET is a polyfunctional cytokine that affects monocytes as well as vascular smooth muscle cells, anterior pituitary cells, and renal mesangial cells. In the biologic interface between ischemic or injured endothelium and monocytes, neutrophils, or lymphocytes, ET may play a significant role. 

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