Effective Gene Delivery to Valvular Interstitial Cells Using Adeno-Associated Virus Serotypes 2 and 3

Wong, Fergus F.; Ho, Michelle; Yamagami, Momona; Lam, Michael T.; Grande-Allen, K. Jane; Suh, Junghae

doi:10.1089/ten.tec.2014.0493

Cited by 5 publications

(3 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This virus does infect humans (and other primates) but is not currently known to cause any diseases and only elicits a very mild immune response in humans as demonstrated by phase I clinical trials . AAV2 is also a replication-defective virus (the coding genes for replication are defective, thus preventing further replication and the lytic pathway to cell lysis), making it ideal as a gene-therapy vector. ,− In fact, there are even AAV2 products that are approved (by European Union) for human use in commercial gene therapy, such as Glybera that can control the production of lipoproteinlipase (which is necessary for processing and clearing fat-carrying chylomicron after eating fat-containing foods) . Incredibly, adenovirus vectors have been used in 22% of all gene-therapy clinical trials to date .…”

Section: Viral Librariesmentioning

confidence: 99%

Virus-Derived Peptides for Clinical Applications

2017

View full text Add to dashboard Cite

Novel affinity agents with high specificity are needed to make progress in disease diagnosis and therapy. Over the last several years, peptides have been considered to have fundamental benefits over other affinity agents, such as antibodies, due to their fast blood clearance, low immunogenicity, rapid tissue penetration, and reproducible chemical synthesis. These features make peptides ideal affinity agents for applications in disease diagnostics and therapeutics for a wide variety of afflictions. Virus-derived peptide techniques provide a rapid, robust, and high-throughput way to identify organism-targeting peptides with high affinity and selectivity. Here, we will review viral peptide display techniques, how these techniques have been utilized to select new organism-targeting peptides, and their numerous biomedical applications with an emphasis on targeted imaging, diagnosis, and therapeutic techniques. In the future, these virus-derived peptides may be used as common diagnosis and therapeutics tools in local clinics.

show abstract

Section: Viral Librariesmentioning

confidence: 99%

Virus-Derived Peptides for Clinical Applications

2017

View full text Add to dashboard Cite

show abstract

“…To investigate the role of ECH1 in aortic valve calcification in vivo, we used AAV2‐ECH1 (or AAV2‐empty control) to overexpress ECH1 in ApoE −/− mice by tail vein injection. 17 ECH1 overexpression in the aortic valves was found to be effective (Figure S1A–C ). After 24 weeks, mice in the HCD AAV2‐scr group displayed significantly higher mean transvalvular pressure gradient and peak transvalvular jet velocity, as well as significantly lower aortic valve area (Figure 2A–D ).…”

Section: Resultsmentioning

confidence: 96%

“…To investigate the role of ECH1 in aortic valve calcification in vivo, we used AAV2‐ECH1 (or AAV2‐empty control) to overexpress ECH1 in ApoE −/− mice by tail vein injection 17 . ECH1 overexpression in the aortic valves was found to be effective (Figure ).…”

Section: Resultsmentioning

confidence: 99%

Enoyl coenzyme a hydratase 1 attenuates aortic valve calcification by suppressing Runx2 via Wnt5a/Ca²⁺ pathway

Rao,

Liu,

Qin

et al. 2024

Journal of Cell Communication and Signaling

View full text Add to dashboard Cite

The morbidity and death rates of calcified aortic valves|calcific aortic valve (CAV) disease (CAVD) remain high for its limited therapeutic choices. Here, we investigated the function, therapeutic potential, and putative mechanisms of Enoyl coenzyme A hydratase 1 (ECH1) in CAVD by various in vitro and in vivo experiments. Single‐cell sequencing revealed that ECH1 was predominantly expressed in valve interstitial cells and was significantly reduced in CAVs. Overexpression of ECH1 reduced aortic valve calcification in ApoE−/− mice treated with high cholesterol diet, while ECH1 silencing had the reverse effect. We also identified Wnt5a, a noncanonical Wnt ligand, was also altered when ECH1 expression was modulated. Mechanistically, we found that ECH1 exerted anti‐calcific actions through suppressing Wnt signaling, since CHIR99021, a Wnt agonist, may significantly lessen the protective impact of ECH1 overexpression on the development of valve calcification. ChIP and luciferase assays all showed that ECH1 overexpression prevented Runx2 binding to its downstream gene promoters (osteopontin and osteocalcin), while CHIR99021 neutralized this protective effect. Collectively, our findings reveal a previously unrecognized mechanism of ECH1‐Wnt5a/Ca2+ regulation in CAVD, implying that targeting ECH1 may be a potential therapeutic strategy to prevent CAVD development.

show abstract

Drug Delivery Systems and Cardiovascular Disease

Wang,

Liang,

Duan

et al. 2024

Application of Biomaterials in the Treatment of Cardiovascular Diseases

View full text Add to dashboard Cite

Effective Gene Delivery to Valvular Interstitial Cells Using Adeno-Associated Virus Serotypes 2 and 3

Cited by 5 publications

References 45 publications

Virus-Derived Peptides for Clinical Applications

Virus-Derived Peptides for Clinical Applications

Enoyl coenzyme a hydratase 1 attenuates aortic valve calcification by suppressing Runx2 via Wnt5a/Ca²⁺ pathway

Drug Delivery Systems and Cardiovascular Disease

Contact Info

Product

Resources

About

Effective Gene Delivery to Valvular Interstitial Cells Using Adeno-Associated Virus Serotypes 2 and 3

Cited by 5 publications

References 45 publications

Virus-Derived Peptides for Clinical Applications

Virus-Derived Peptides for Clinical Applications

Enoyl coenzyme a hydratase 1 attenuates aortic valve calcification by suppressing Runx2 via Wnt5a/Ca2+ pathway

Drug Delivery Systems and Cardiovascular Disease

Contact Info

Product

Resources

About

Enoyl coenzyme a hydratase 1 attenuates aortic valve calcification by suppressing Runx2 via Wnt5a/Ca²⁺ pathway