Arteries smooth muscle cells

J mohara M, Takasaki J, Matsumoto M> Matsumoto S-I, Saito X Soga X Matsushime H, Furuichi K Functional characterization of cysteinyl leukotriene CysLT2 receptor on human coronary artery smooth muscle cells. Biochem Biophys Res Commun 2001 287 1088. 

The intima of the arterial wall contains hyaluronic acid and chondroitin sulfate, dermatan sulfate, and heparan sulfate proteoglycans. Of these proteoglycans, dermatan sulfate binds plasma low-density lipoproteins. In addition, dermatan sulfate appears to be the major GAG synthesized by arterial smooth muscle cells. Because it is these cells that profiferate in atherosclerotic lesions in arteries, dermatan sulfate may play an important role in development of the atherosclerotic plaque. 

Evidence from cellular studies in vitro initially showed how oxidative processes could play a central role in the pathological changes involved in the genesis of atherosclerosis. LDL can be oxidatively modified in culture by a range of cell types including endothelial cells (Henriksen et a.1., 1981), arterial smooth muscle cells... 

Heinecke, J.W., Rosen, H. and Chait, A. (1984). Iron and copper promote modification of low density lipoprotein by human arterial smooth muscle cells in culture. J. Clin. Invest. 74, 1890-1894. 

Holland et al. [125] have shown that the potent vascular smooth muscle cell mitogen and phospholipase A2 activator thrombin stimulated superoxide production in human endothelial cells, which was inhibited by the NADPH oxidase inhibitors. Similarly, thrombin enhanced the production of oxygen species and the expression of )Alphos and Rac2 subunits of NADPH oxidase in VSMCs [126,127]. Greene et al. [128] demonstrated that the activator of NO synthase neuropeptide bradykinin is also able to stimulate NADPH oxidase in VSMCs. Similar to XO, NADPH oxidase enhanced superoxide production in pulmonary artery smooth muscle cells upon exposure to hypoxia [129]. 

Oxidized LDL are considered to be one of the major factors associated with the development of atherosclerosis. The earliest event is the transport of LDL into the arterial wall where LDL, being trapped in subendothelial space, are oxidized by oxygen radicals produced by endothelial and arterial smooth muscle cells. The oxidation of LDL in the arterial wall is affected by various factors including hemodynamic forces such as shear stress and stretch force. Thus, it has been shown [177] that stress force imposed on vascular smooth muscle cells incubated with native LDL increased the MDA formation by about 150% concomitantly with the enhancement of superoxide production. It was suggested that oxidation was initiated by NADPH oxidase-produced superoxide and depended on the presence of metal ions. 

Bhalla RC, Toth KF, Bhatty RA, Thompson LP, Sharma RV (1997) Estrogen reduces proliferation and agonist-induced calcium increase in coronary artery smooth muscle cells. Am J Physiol 272 H 1996-2003... 

Lavigne MC, Ramwell PW, Clarke R (1999) Inhibition of estrogen receptor function promotes porcine coronary artery smooth muscle cell proliferation. Steroids 64 472-480... 

Asada Y, Yamazawa T, Hirose K, Takasaka T, lino M 1999 Dynamic Ca2+ signalling in rat arterial smooth muscle cells under the control of local renin-angiotensin system. J Physiol 521 497-505... 

James PF, Grupp IL, Grupp G et al 1999 Identification of a specific role for the Na,K-ATPase a2 isoform as a regulator of calcium in the heart. Mol Cell 3 555—563 Janiak R, Wilson, SM, Montague S, Hume JR 2001 Heterogeneity of calcium stores and elementary release events in canine pulmonary arterial smooth muscle cells. Am J Physiol 280 C22-C33... 

Fung and colleagues examined the metabolic conversion of organic nitrates in sub-cellular fractions of bovine coronary artery smooth muscle cells [66, 67]. They found NO-generating capacity to be present in membrane fractions and, with the use of marker enzymes, identified plasma membrane as the primary location. The enzyme involved in bioconversion was not glutathione-S-transferase [68] and differed from those that catalyse activation of organic nitrites [69]. Partial purification [70] established that the molecular sizes of the native enzyme and subunits were approximately 200 kDa and 58 kDa respectively, and that enzymic activity depends on the presence of a free thiol group. 

Bachem, M.G., Wendelin, D., Schneiderhan, W., Haug, C., Zom, U., Gross, H.J., Schmid-Kotsas, A., and Gmnert, A., 1999, Depending on their concentration oxidized low density lipoproteins stimulate extracellular matrix synthesis or induce apoptosis in human coronary artery smooth muscle cells, Clin Chem Lab Med. 37 319-326. 

Bjorkemd, B., and Bjorkemd, S., 1996b, Contrary effects oflightly and strongly oxidized LDL with potent promotion of growth versus apoptosis on arterial smooth muscle cells, macrophages, and fibroblasts, Arterioscler Thromb Vase Biol. 16 416-424. 

IHC shows constitutive and inducible CYPIBI in artery smooth muscle cells, leptomeninges, cerebral arteries/arterioles, and ependymal cells (Granberg et al., 2003). 

Axel DI, Kunert W, Goggehnann C, et al. Pachtaxel inhibits arterial smooth muscle cell proliferation and migration in vitro and in vivo using local drug dehvery. Circulation 1997 96 636-645. 

Hefton. Tobacco constituents are mitogenic for arterial smooth-muscle cells. Am J Pathol 1985 120(1) 1-5. 

In addition to their antianginal (see Chapter 12) and antiarrhythmic effects (see Chapter 14), calcium channel blockers also reduce peripheral resistance and blood pressure. The mechanism of action in hypertension (and, in part, in angina) is inhibition of calcium influx into arterial smooth muscle cells. 

Serotonin (5-HT) produces a rapid elevation of superoxide that stimulates the mitogenesis of bovine pulmonary artery smooth muscle cells (SMCs). EGb scavenges superoxide elevated by 5-HT, hence preventing 5-HT-induced mitogenesis on both SMCs and Chinese hamster lung fibroblasts. These results indicate that EGb inhibits the cellular transduction signaling process that leads to mitogenesis, as a result of its antioxidant activity [141]. 

Saponara S, Sgaragli G, Fusi F. 2002. Quercetin as a novel activator of L-type Ca2 + channels in rat tail artery smooth muscle cells. Br J Pharmacol 135 1819-1827. 

Leung, D. Y. M., Glagov, S., and Mathews, M. B. (1976). Cyclic stretching stimulates synthesis of matrix components by arterial smooth muscle cells in vitro. Science 191, 475-477. 

Figure 12.9 Endothelial cell-specific nuclear import of plasmids. Growth-arrested African Green Monkey kidney epithelial cells (TC7), human pulmonary artery smooth muscle cells (HSMCs) and human umbilical vein endothelial cells (HUYECs) were microinjected in the nucleus (top) and cytoplasm with CMV-driven, GFP-expressing plasmids containing either no additional sequences (open bars), the SV40 enhancer (striped bars), or the flk-1 promoter (shaded bars). Eight hours after injection, the cells were visualized for GFP expression by fluorescence microscopy. Whereas all three plasmids supported GFP expression when delivered into the nucleus of all three cell types, only the SV40 enhancer mediated nuclear import and gene expression in all cells when injected into the cytoplasm. As predicted, the flk-1 promoter caused import and expression only in cells in which transcription factors necessary for its expression and import were made, namely endothelial cells.

Monkey kidney epithelial cells (TC7), human pulmonary artery smooth muscle cells... 

Sweeney, M., Yu, Y., Platoshyn, O., Zhang, S., McDaniel, S. S. and Yuan, J. X., 2002, Inhibition of endogenous TRP1 decreases capacitative Ca2+ entry and attenuates pulmonary artery smooth muscle cell proliferation. Am J Physiol Lung Cell Mol Physiol 283, L144—55. 

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