Smooth muscle cells , proliferation

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. 

Chandrasekar B, Bysani S, Mummidi S. CXCL16 signals via Gi, phosphatidylino-sitol 3-kinase, Akt, I kappa B kinase, and nuclear factor-kappa B and induces cell-cell adhesion and aortic smooth muscle cell proliferation. J Biol Chem 2004 279(5) 3188-3196. 

Block of vascular smooth muscle cell proliferation Rat ICI 164384 (Cathapermal et al. 1998)... 

By acting on the vessel wall, estradiol significantly inhibited superoxide anion-induced vascular smooth muscle cell proliferation, whereas the pure antiestrogen ICI 164384 reversed the inhibitory effect of estradiol (Cathapermal et al. 1998). Fulvestrant also reversed the estradiol-induced increase in blood flow in rabbit aorta (Hegele-Hartung et al. 1997). 

Cathapermal S, LavigneMC, Leong-Son M,Alibadi T, Ramwell PW (1998) Stereoisomer-specific inhibition of superoxide anion-induced rat aortic smooth-muscle cell proliferation by 17beta-estradiol is estrogen receptor dependent. J Cardiovasc Pharmacol 31 499-505... 

Espinosa E, Oemar BS, Luscher TF (1996) 17 beta-Estradiol and smooth muscle cell proliferation in aortic cells of male and female rats. Biochem Biophys Res Commun 221 8-14... 

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

Ricciardelli C, Horsfall DJ, Sykes PJ, Marshall VR, Tilley WD (1994) Effects of oestradiol-17 beta and 5 alpha-dihydrotestosterone on guinea-pig prostate smooth muscle cell proliferation and steroid receptor expression in vitro. J Endocrinol 140 373-383... 

Yue TL, Vickery-Clark L, Louden CS, Gu JL, Ma XL, Narayanan PK, Li X, Chen J, Storer B, Willette R, Gossett KA, Ohlstein EH (2000) Selective estrogen receptor modulator idoxifene inhibits smooth muscle cell proliferation, enhances reendothelial-ization, and inhibits neointimal formation in vivo after vascular injury. Circulation 102(Suppl 3) III281—288... 

JLompre I would like to present some of our results describing the changes that occur to cells in culture. My concern is primarily with the organization of the SR when vascular smooth muscle cells proliferate in culture. This is of interest because of the importance of smooth muscle cell proliferation in atherosclerosis and restenosis. Freshly dissociated cells or those that have been cultured for just one... 

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. 

Tulis DA, Mnjoyan ZH, Schiesser RL, et al. Adenoviral gene transfer of fortilin attenuates neointima formation through suppression of vascular smooth muscle cell proliferation and migration. Circulation. Jan 7 2003 107(1) 98-105. 

Alcocer, F., Whitley, D., Salazar-Gonzalez, J.F., Jordan, W.D., Sellers, M.T., Eckhoff, D.E., Suzuki, K., MacRae, C., and Bland, K.L., Quercetin inhibits human vascular smooth muscle cell proliferation and migration. Surgery, 131, 198, 2002. 

Araim, O., Ballantyne, J., Waterhouse, A.L., and Sumpio, B.E., Inhibition of vascular smooth muscle cell proliferation with red wine and red wine polyphenols, J. Vase. Surg., 35, 1226, 2002. 

Locher, R., Emmanuele, L., Suter, P.M., Vetter, W., and Barton, M., Green tea polyphenols inhibit human vascular smooth muscle cell proliferation stimulated by native low-density lipoprotein, Eur. J. Pharmaeol, 434, 1, 2002. 

Kim TJ, Kim JH, Jin YR, Yun YP. 2006. The inhibitory effect and mechanism of luteolin 7-glucoside on rat aortic vascular smooth muscle cell proliferation. Arch Pharm Res 29 67-72. 

Jarvis, T.C., Alby, L.J., Beaudry, A.A., Wincott, F.E., Beigelman, L., McSwiggen, J.A., Usman, N. and Stinchcomb, D.T. (1996a) Inhibition of vascular smooth muscle cell proliferation by ribozy mes that cleave c-myb mRNA. RNA, 2,419—428. 

Lipskaia, L., del Monte, F., Capiod, T., Yacoubi, S., Hadri, L., Hours, M., Hajjar, R. J. and Lompre, A. M., 2005, Sarco/endoplasmic reticulum Ca2+-ATPase gene transfer reduces vascular smooth muscle cell proliferation and neointima formation in die rat. Circ Res 97, 488—95. 

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. 

Atorvastatin calcium possesses an anti-inflammatory property and reduces the accumulation of inflammatory cells in the atherosclerotic plaques. The drug also inhibits the vascular smooth muscle cell proliferation a key event in the atherogenesis. Atorvastatin also inhibits the platelet function, thereby limiting both the atherosclerosis and the superadded thrombosis and also improves the vascular endothelial function, largely through the amplification of nitric oxide (NO) generation [3-5]. 

J. Jozefonvicz. 1996. Conjugates of insulin with copolymers of N-(2-hydroxypropyl) methacrylamide effects on smooth muscle cell proliferation. J. Biomed. Mater-Res. 31 265-272. 

The thrombotic disorders include atherothrombosis, endothelial dysfunction, hypercoagulable states, and the thrombophilias. Atherothrombosis or atherosclerosis is a systemic disease of the vessel wall occuring in the aorta, carotid, coronary, and peripheral arteries. The associated inflammatory response is mediated by macrophages and T-lymphocytes with continued smooth muscle cell proliferation, The levels of endothelin-l (ET-I), an extremely potent... 

Pemirolast Inhibition of smooth muscle cell proliferation and migration Ohsawa (55) Low restenosis and neointimal hyperplasia... 

Acute vessel recoil, chronic remodeling, and intimal hyperplasia were the mechanisms involved in this process (1-4). However, after the introduction of stents in the daily practice during interventional procedures, intimal hyperplasia became the mechanism associated in the pathophysiology of in-stent restenosis (5-9). Therefore, its prevention should be related with therapies that inhibit smooth muscle cell proliferation. 

Animal data suggest that the degree of neointimal proliferation formed after stent implantation is mediated by smooth muscle cell proliferation and occurs during the first two weeks... 

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