The Role of Gene Therapy for Intimal Hyperplasia of Bypass Grafts

Cable, David G.; Caccitolo, James A.; Caplice, Noel M.; O’Brien, Timothy J.; Simari, Robert D.; Daly, Richard C.; Dearani, Joseph A.; Mullany, Charles J.; Orszulak, Thomas A.; Schaff, Hartzell V.

doi:10.1161/01.cir.100.suppl_2.ii-392

Cited by 45 publications

(35 citation statements)

References 22 publications

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“…This approach is applicable to gene delivery ex vivo, for example, to endothelial cells prior to transplantation of organs such corneas [40][41][42][43] or to autologous transplantation of vessels in procedures such as coronary artery or peripheral vascular bypass grafts [44,45]. It is also a step in the production of totally targeted non-viral vectors.…”

Section: Discussionmentioning

confidence: 99%

Antibody targeted gene transfer to endothelium

Tan

Manunta

Ardjomand

et al. 2002

The Journal of Gene Medicine

106

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We have shown that our novel vector is capable of in vitro and ex vivo gene delivery to cells and human tissues including cornea, artery and vein. In particular, an Ab against E-selectin was effective at selectively delivering genes to activated endothelial cells expressing the adhesion molecule. Such a strategy will have applications for targeting these tissues prior to transplantation or autologous grafting, and, in the longer term, may allow in vivo targeting of gene therapy to inflammatory sites.

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Section: Discussionmentioning

confidence: 99%

Antibody targeted gene transfer to endothelium

Tan

Manunta

Ardjomand

et al. 2002

The Journal of Gene Medicine

106

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“…Gene Therapy (2001) 8, 668-676. potential therapies. 6 To date, a number of studies have targeted different mechanisms involved in the progression of vein graft neointimal thickening, [7][8][9][10][11][12][13] and recently, clinical trials have been initiated. 14 Mann et al 10,11 modulated the cell cycle using antisense oligonucleotides targeting proliferating cell nuclear antigen (PCNA) or cell division cycle 2 (cdc 2) kinase, and reduced neointimal hyperplasia 10 through enhanced nitric oxide bioavailabilty and reduced monocyte adhesion and vascular cell adhesion molecule-1 (VCAM-1) expression.…”

Section: Introductionmentioning

confidence: 99%

Wild-type p53 gene transfer inhibits neointima formation in human saphenous vein by modulation of smooth muscle cell migration and induction of apoptosis

et al. 2001

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Patency of autologous human saphenous vein coronary artery bypass grafts (CABG) is compromised by intimal thickening and superimposed atherosclerosis, caused by migration of vascular smooth muscle cells (SMC) to the intima where they proliferate. Here, using adenoviral transfer, we have targeted SMCs using wild-type p53 (wt p53) overexpression. Initial in vitro analyses demonstrated that wt p53 overexpression had no effect on SMC proliferation but promoted apoptosis, which was inhibited by co-expression of bcl2 or crmA. Wt p53 inhibited SMC invasion through reconstituted matrices, a phenotype not affected by bcl2 or crmA. Overexpression of wt p53 in human saphenous vein

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“…Ex vivo eNOS gene transfer using adenoviral vectors increased NO production and NO-dependent relaxation and inhibit intimal hyperplasia in cultured human saphenous veins (42,43). Gene transfer of eNOS has also been carried out in autologous femoral vein grafts prior to their implantation to ipsilateral femoral arteries in a dog model (44).…”

Section: -4 Autograft Vasculopathymentioning

confidence: 99%

Nitric Oxide Synthase Gene Therapy for Cardiovascular Disease

Chen

Ren

Miao

2002

Japanese Journal of Pharmacology

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ABSTRACT-Gene therapy refers to the transfer of specific genes to the host tissue to intervene in a disease process, with resultant alleviation of the symptoms of a particular disease. Cardiovascular gene transfer is not only a powerful technique for studying the function of specific genes in cardiovascular biology and pathobiology, but also a novel and promising strategy for treating cardiovascular diseases. Since the mid1990s, nitric oxide synthase (NOS), the enzyme that catalyzes the formation of nitric oxide (NO) from L-arginine, has received considerable attention as a potential candidate for cardiovascular gene therapy, because NO exerts critical and diverse functions in the cardiovascular system, and abnormalities in NO biology are apparent in a number of cardiovascular disease processes including cerebral vasospasm, atherosclerosis, postangioplasty restenosis, transplant vasculopathy, hypertension, diabetes mellitus, impotence and delayed wound healing. There are three NOS isoforms, i.e., endothelial (eNOS), neuronal (nNOS) and inducible (iNOS). All three NOS isoforms have been used in cardiovascular gene transfer studies with encouraging results. This review will discuss the rationale of NOS gene therapy in different cardiovascular disease settings and summarize the results of experimental NOS gene therapy from various animal models of cardiovascular disease to date.

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The Role of Gene Therapy for Intimal Hyperplasia of Bypass Grafts

Cited by 45 publications

References 22 publications

Antibody targeted gene transfer to endothelium

Antibody targeted gene transfer to endothelium

Wild-type p53 gene transfer inhibits neointima formation in human saphenous vein by modulation of smooth muscle cell migration and induction of apoptosis

Nitric Oxide Synthase Gene Therapy for Cardiovascular Disease

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