Catheter-based adenovirus-mediated local intravascular gene delivery of a soluble TGF-β type II receptor using an Infiltrator in porcine coronary arteries: efficacy and complications

Chung, Ick Mo; Ueno, Hikaru; Pak, Youngmi Kim; Kim, Joon‐Woo; Choi, Donghoon; Shin, Gil Ja; Yang, Woo Ick; Jang, Yangsoo

doi:10.1038/emm.2002.42

Cited by 13 publications

(9 citation statements)

References 37 publications

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“…HepG2 cells were infected for 48 h with adenoviruses expressing either LacZ (AdLacZ) (Chung et al, 2002) or PGC-1α with (His)6-tag at its N-terminus (AdPGC-1) at a multiplicity of infection (moi) of 50 and harvested for Western blotting or for RT-PCR analysis. In some cases, the infected cells in serum free media containing 0.5% FBS were treated with the inhibitor of p38-MAPK, SB202190 (20 μM), for 24 h and harvested for RT-PCR or Northern analysis.…”

Section: Adenovirus Infectionmentioning

confidence: 99%

Sterol-independent repression of low density lipoprotein receptor promoter by peroxisome proliferator activated receptor γ coactivator-1α (PGC-1α)

2009

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Abbreviations: E2, 17β-ethinyl estradiol; EMSA, electrophoretic mobility shift assay; ER, estrogen receptor; ERE, estrogen response element; LDLR, low density lipoprotein receptor; moi, multiplicity of infection; p38-MAPK, p38-mitogen activated protein kinase; PEPCK, phosphoenolpyruvate carboxykinase; PGC-1α, PPARγ coactivator-1α; PPARγ, peroxisome proliferator activated receptor γ; SRE-1, sterol regulatory element-1; SREBP, SRE-1 binding

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Section: Adenovirus Infectionmentioning

confidence: 99%

Sterol-independent repression of low density lipoprotein receptor promoter by peroxisome proliferator activated receptor γ coactivator-1α (PGC-1α)

2009

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“…The medial layer revealed mild local thickening without luminal narrowing [17]. Several preclinical studies have established evidence that infiltrator catheters can be used for gene transfer to the vasculature [18,19]. Wang et al [18] demonstrated successful gene transfer using recombinant adenovirus, encoding inducible nitric oxide synthase in porcine coronary arteries.…”

Section: Infiltrator Catheters (Direct)mentioning

confidence: 99%

Current status of catheter- and stent-based gene therapy

Sharif¹,

Daly²,

Crowley³

et al. 2004

Cardiovascular Research

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Significant progress has been made in the field of cardiovascular gene therapy over the past decade. Animal models of human disease have helped in identifying potential therapeutic genes and have also assisted in the evaluation of an ideal vector. A number of percutaneous catheter systems have been used in animal models with limited success. Stents represent an attractive alternative for localized gene delivery, as they provide a platform for prolonged gene elution and efficient transduction of opposed arterial walls. This gene delivery strategy has the potential to decrease the systemic spread of the viral vectors and hence a reduced host immune response. Both synthetic and naturally occurring stent coatings have shown potential to allow prolonged gene elution with no significant adverse reaction. However, further animal studies are required to evaluate the compatibility of stent coatings, vector solutions, and the arterial wall as well as assessment of the feasibility of this approach to achieve the full potential of gene therapy.

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“…These observations differ from studies of TGF-b1 in noncoronary vessels, where TGF-b1 increased neointima formation within normal (Nabel et al, 1993;Schulick et al, 1998) and injured (Kanzaki et al, 1995) arteries, while antagonists of TGF-b1 reduced neointima formation (Wolf et al, 1994;Smith et al, 1999;Yamamoto et al, 2000;Ando et al, 2004;Ikeda et al, 2004;Yao et al, 2009). The apparent discrepancy between observations made in coronary arteries and those made in other vessels might be the consequence of the location of transgene expression: the Infiltrator catheter (used by us and by Chung et al) delivers material principally to the adventitia (Kingston et al, 2001Chung et al, 2002b), while studies of TGF-b1 antagonism in noncoronary arteries have used endoluminal routes that deliver antagonists to the luminal aspect of the artery (Wolf et al, 1994;Smith et al, 1999;Yamamoto et al, 2000;Ando et al, 2004;Ikeda et al, 2004;Yao et al, 2009). Other possibilities might account for these observations, however.…”

Section: Introductionmentioning

confidence: 79%

“…All other studies of antagonism of TGF-b in the coronary arteries have failed to demonstrate reduced neointima formation (Paiement et al, 1998;Chung et al, 2002bChung et al, , 2010. These observations differ from studies of TGF-b1 in noncoronary vessels, where TGF-b1 increased neointima formation within normal (Nabel et al, 1993;Schulick et al, 1998) and injured (Kanzaki et al, 1995) arteries, while antagonists of TGF-b1 reduced neointima formation (Wolf et al, 1994;Smith et al, 1999;Yamamoto et al, 2000;Ando et al, 2004;Ikeda et al, 2004;Yao et al, 2009).…”

Section: Introductionmentioning

confidence: 92%

Periluminal Expression of a Secreted Transforming Growth Factor-β Type II Receptor Inhibits In-Stent Neointima Formation Following Adenovirus-Mediated Stent-Based Intracoronary Gene Transfer

et al. 2014

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Transforming growth factor-β1 (TGF-β1) has been shown unequivocally to enhance neointima formation in carotid and ileo-femoral arteries. In our previous studies, however, TGF-β1 expression in coronary arteries actually reduced neointima formation without affecting luminal loss postangioplasty, while expression of a TGF-β1 antagonist (RIIs) in balloon-injured coronary arteries reduced luminal loss without affecting neointima formation. These observed effects may be a consequence of the mode of coronary artery gene transfer employed, but they may also represent differences in the modes of healing of coronary, carotid, and ileo-femoral arteries after endoluminal injury. To help clarify whether a gene therapy strategy to antagonize TGF-β might have application within the coronary vasculature, we have investigated the effect of high-level periluminal expression of RIIs using stent-based adenovirus-mediated intracoronary gene transfer. Porcine coronary arteries were randomized to receive a custom-made CoverStent preloaded with saline only, or with 1×10(9) infectious units of adenovirus expressing RIIs or β-galactosidase (lacZ). Vessels were analyzed 28 days poststenting, at which time angiographic in-stent diameter was significantly greater in RIIs-treated arteries, and in-stent luminal loss significantly reduced. Computerized morphometric minimum in-stent lumen area was ~300% greater in RIIs-exposed vessels than in lacZ or saline-only groups. This was because of significantly reduced neointima formation in the RIIs group. RIIs had no demonstrable effect on cellular proliferation or apoptosis, but greater normalized neointimal/medial collagen content was observed in RIIs-exposed arteries. These data highlight the qualitatively similar effect of TGF-β antagonism on neointima formation in injured coronary and noncoronary arteries, and suggest that since cellular proliferation is unaffected, TGF-β1 antagonism might prevent in-stent restenosis without the delayed healing that is associated with drug-eluting stents in current clinical use.

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Catheter-based adenovirus-mediated local intravascular gene delivery of a soluble TGF-β type II receptor using an Infiltrator in porcine coronary arteries: efficacy and complications

Cited by 13 publications

References 37 publications

Sterol-independent repression of low density lipoprotein receptor promoter by peroxisome proliferator activated receptor γ coactivator-1α (PGC-1α)

Sterol-independent repression of low density lipoprotein receptor promoter by peroxisome proliferator activated receptor γ coactivator-1α (PGC-1α)

Current status of catheter- and stent-based gene therapy

Periluminal Expression of a Secreted Transforming Growth Factor-β Type II Receptor Inhibits In-Stent Neointima Formation Following Adenovirus-Mediated Stent-Based Intracoronary Gene Transfer

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