Download PDF by Alan D. Simon M.D., Mark K. Warshofsky M.D. (auth.), LeRoy: Applications of Antisense Therapies to Restenosis

By Alan D. Simon M.D., Mark K. Warshofsky M.D. (auth.), LeRoy E. Rabbani M.D. (eds.)

ISBN-10: 1461373611

ISBN-13: 9781461373612

ISBN-10: 1461551838

ISBN-13: 9781461551836

Restenosis, the proliferation of tender muscle cells (SMC) that line blood vessels, usually follows angioplasty. regardless of advances in cardiology, restenosis keeps to impact as much as forty% of the over 500,000 sufferers who endure angioplasty every year.
Applications of Antisense cures to Restenosis is the 1st quantity to handle the opportunity of utilizing antisense treatments to inhibit the restenosis that happens after percutaneous transluminal angioplasty and coronary stenting. The paintings severely examines the appliance of assorted antisense treatments for inhibiting restenosis.

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7 The inflammatory cells and vasa vasorum are found in the adventitia in unstable coronary syndromes and after PTCA. 14,15,16 These scattered observations indirectly suggest that adventitia plays more than a passive role during vascular repair. Transcatheter coronary interventions often result in medial dissection and possible exposure of the adventitia to the lumen. 17 In a porcine model, this initiates a chain of events reminiscent of the wound healing process. 18 In contrast to non-coronary vascular beds, coronary medial SM cells show a low level of cell proliferation.

37 70 ~ 60 ... SO • Adventitia . '0 ,540 c =30 e ~ 20 e J:>. 10 0 +-'- -- - . 14 days 18 d"Y' Figure 1. Time course of cell proliferation (pCNA immunostaining) in injured porcine coronary arteries. Each bar represents mean±SEM (n=3-4 vessels/time point). 19 Figure 2. Photomicrograph depicting expression of a-SM actin by fibroblasts within the adventitia (a) at 8 days after injury. n denotes neointima. Magnification 90x. Similar to their non-vascular counterparts (eg, wound healing myofibroblasts), adventitial cells are actively involved in the synthesis of extracellular matrix in order to repair the injured vessel.

53. 54. 55. 56. 57. 58. 59. 60. 61. 62. 63. 64. 65. 66. Clowes A, Reidy MA, and Clowes MM. Mechanisms of stenosis after arterial injury. Lab Invest, 1983;49(2):208. Thomas W A, and Kim DN. Biology of disease: atherosclerosis as a hyperplastic and/or neoplastic process. Lab Invest, 1983;48:245. Nathan C and Sporn M. Cytokines in context. J Cell BioI, 1991;113(5):981. 'tctor beta is produced by co-cultures of endothelial cells and pericytes. Proc Natl Acad Sci USA, 1989;86:4544. Robert~ AB and Sporn M.

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Applications of Antisense Therapies to Restenosis by Alan D. Simon M.D., Mark K. Warshofsky M.D. (auth.), LeRoy E. Rabbani M.D. (eds.)

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