ArticleMolecular therapy. Nucleic acids2013
Long-term Expression of Apolipoprotein B mRNA-specific Hammerhead Ribozyme via scAAV8.2 Vector Inhibits Atherosclerosis in Mice.
Article in Molecular therapy. Nucleic acids, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- A Critical Role of PCSK9 in Mediating IL-17-Producing T Cell Responses in Hyperlipidemia.Immune network · 2019Article
- Dynamic Actin Reorganization and Vav/Cdc42-Dependent Actin Polymerization Promote Macrophage Aggregated LDL (Low-Density Lipoprotein) Uptake and Catabolism.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- PCSK9 deficiency reduces atherosclerosis, apolipoprotein B secretion, and endothelial dysfunction.Journal of lipid research · 2018Article
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Target substrate-specific hammerhead ribozyme cleaves the specific mRNA efficiently and results in the inhibition of gene expression. In humans, overproduction of apolipoprotein B (apoB) is positively associated with premature coronary artery diseases. The goal of this study is to demonstrate that long-term reduction of apoB gene expression using hammerhead ribozyme would result in inhibition of atherosclerosis development. We designed two hammerhead ribozymes targeted at the nucleotides of apoB mRNA GUC(2326) (designated RB1) and GUA(6679) (designated RB15), and we used self-complementary adeno-associated virus 8.2 (scAAV8.2) vector to deliver these active ribozymes of RB1, RB15, combination of RB1/RB15, and an inactive hammerhead ribozyme RB15 mutant to atherosclerosis-prone LDb mice (Ldlr(-/-)Apobec1(-/-)). LDb mice lack both low density lipoproteins (LDL) receptor (Ldlr(-/-)) and apoB mRNA editing enzyme (Apobec1(-/-)) genes and develop atherosclerosis spontaneously. After the RB1, RB15, or combination of RB1/RB15 ribozymes treatment, the LDb mice had significantly decreased plasma triglyceride and apoB levels, resulting in markedly decreased of atherosclerotic lesions, Furthermore, the active ribozymes treatment decreased the levels of diacylglycerol acyltransferase 1 (Dgat1) mRNA and the levels of multiple diacylglycerol (DAG) molecular species. These results provide the first evidence that decreased apoB levels results to reduction of Dgat1 expression and triglyceride levels (TAG), which had a significant impact on the development of atherosclerosis.Molecular Therapy-Nucleic Acids (2013) 2, e125; doi:10.1038/mtna.2013.53; published online 1 October 2013.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.