ArticleGene therapy1999
Adenovirus-mediated delivery of the Gax transcription factor to rat carotid arteries inhibits smooth muscle proliferation and induces apoptosis.
Article in Gene therapy, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 45 citations in OpenAlex.
- Ref-1 protects against FeClThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021Article
- Article
- CRCT1 regulated by microRNA-520 g inhibits proliferation and induces apoptosis in esophageal squamous cell cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Gax regulates human vascular smooth muscle cell phenotypic modulation and vascular remodeling.American journal of translational research · 2016Article
- Crosstalk between TGF-β/Smad3 and BMP/BMPR2 signaling pathways via miR-17-92 cluster in carotid artery restenosis.Molecular and cellular biochemistry · 2014Article
- Transcription factor and kinase-mediated signaling in atherosclerosis and vascular injury.Current atherosclerosis reports · 2006Review
- The cell cycle: a critical therapeutic target to prevent vascular proliferative disease.The Canadian journal of cardiology · 2006Review
- Characterization of Mesenchyme Homeobox 2 (MEOX2) transcription factor binding to RING finger protein 10.Molecular and cellular biochemistry · 2005Article
- Transcriptional stimulation by the DNA binding protein Hap46/BAG-1M involves hsp70/hsc70 molecular chaperones.Nucleic acids research · 2003Article
- Effect of percutaneous adenovirus-mediated Gax gene delivery to the arterial wall in double-injured atheromatous stented rabbit iliac arteries.Gene therapy · 2000Article
- Vectors for gene therapy of cardiovascular disease.Current cardiology reports · 2000Review
- Gene therapy for restenosis.Current cardiology reports · 2000Review
- Regulation of smooth muscle cell migration and integrin expression by the Gax transcription factor.The Journal of clinical investigation · 1999Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Adenovirus-mediated gene delivery in animal models of vascular injury has provided insights into the mechanisms underlying vessel wall pathologies. We have previously demonstrated that overexpression of the Gax transcription factor inhibits neointimal formation in rat and rabbit models of arterial injury. Here, we evaluate potential mechanisms for the reduction in stenotic lesion size due to Gax overexpression. At 3, 7 and 14 days after injury the Ad-Gax-infected arteries displayed a marked decrease in medial vascular smooth muscle cell number (3 days, 54% reduction P < 0.01; 7 days, 41% reduction P < 0.003; 14 days, 49% reduction P < 0.02). At 3 days after injury, PCNA expression was attenuated in the Ad-Gax-treated vessels compared with control vessels (65% reduction P < 0.02), indicating a reduction in cellular proliferation. At 7 days and 14 days after injury Ad-Gax-infected arteries exhibited elevated number of TUNEL-positive medial VSMCs compared with control-treated arteries (7 days, 9.2-fold increase P < 0.03; 14 days, 17.2-fold increase P < 0.03), indicating an induction of apoptotic cell death. These data suggest that deregulated Gax expression induces first cell cycle arrest and then apoptosis in the vascular smooth muscle cells that contribute to the neointimal layer. Therefore, the efficacy of this therapeutic strategy appears to result from the ability of the Gax transcriptional regulator to modulate multiple cellular responses.
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