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Applications of Antisense Therapies to Restenosis pp 71–98Cite as

Vascular Antisense Therapy Directed Against c-myc, c-myb and PCNA

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Part of the book series: Perspectives in Antisense Science ((DARE,volume 3))

Abstract

Normally quiescent and contractile in phenotype (Reviewed in [1]), vascular smooth muscle cells {VSMC} contribute to the structural integrity of the vascular tree and are critical effector organs in the regulation of blood pressure and tissue perfusion. It is this phenotype that allows endothelial-derived, circulating, and autonomic signals to co-ordinate vasomotor tone through direct effects on VSMC contractility. However, in response to a variety of injurious stimuli, normally quiescent and contractile VSMC can be transformed into migratory and proliferating VSMC that expand and remodel their surrounding matrix [1–4]. Indeed, atherosclerosis, hypertension and other models of arterial injury are typified by proliferating and synthetic VSMC causing neointimal formation, medial hypertrophy, and ultimately lumen encroachment [5–8].

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Authors
  1. Mansoor Husain M.D.
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  2. Michael Simons M.D.
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Editors and Affiliations

  1. Cardiology Division, Columbia University College of Physicians and Surgeons, New York, NY, USA

    LeRoy E. Rabbani M.D. (Assistant Professor of Medicine) (Assistant Professor of Medicine)

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Husain, M., Simons, M. (1999). Vascular Antisense Therapy Directed Against c-myc, c-myb and PCNA. In: Rabbani, L.E. (eds) Applications of Antisense Therapies to Restenosis. Perspectives in Antisense Science, vol 3. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5183-6_5

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