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(Hypertension. 2009;53:751.)
© 2009 American Heart Association, Inc.
Editorial Commentaries |
From the Department of Environmental and Molecular Toxicology (J.C.B.), North Carolina State University, Raleigh; Cantox Health Sciences International (J.W.C.), Mississauga, Ontario, Canada; and the Division of Intramural Research (D.C.Z.), National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC.
Correspondence to Darryl C. Zeldin, NIH/NIEHS, PO Box 12233, Research Triangle Park, NC 27709. E-mail zeldin@niehs.nih.gov
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Nanotechnology offers great potential benefits for drug delivery and therapy of respiratory and systemic diseases. Nanoparticles (NPs) have been of significant interest for some time because they can be designed to simultaneously carry a drug payload, specifically target features of diseased tissues, and carry an imaging molecule to track drug accumulation and clearance in tissues. Moreover, they can be engineered to tailor drug delivery and improve pharmacokinetics. A variety of NPs have been investigated in experimental animal models as tools to improve the delivery and therapeutic efficacy of drugs or genes delivered to the lung or other organ systems.1 The nanotechnology platform for drug delivery contains a number of very different types of nanostructures with widely varying properties. Examples of these NPs include dendrimers, fullerenes, carbon nanotubes, and polymeric NPs.
In this issue of Hypertension, Kimura et al2 report that nuclear factor
B (NF-
B) decoy oligodeoxynucleotides (ODNs) encapsulated in poly-(ethylene glycol)-block-lactide/glycolide copolymer NPs and delivered to the lungs of rats by intratracheal instillation reduced pulmonary arterial hypertension (PAH) induced by monocrotaline (MCT). They showed that NP-encapsulated NF-
B decoy, visualized by fluorescein isothiocyanate labeling, reached the distal regions of the lungs and was present in alveolar macrophages and small pulmonary arteries for
14 days after a single instillation. The small pulmonary arteries were also found to be a site of NF-
B activation and NF-
B–dependent inflammatory cytokine production (monocyte chemoattractant protein 1, interleukin 1, and tumor necrosis factor
) in patients with PAH and in
Related Article:
B Decoy Into Lungs Ameliorates Monocrotaline-Induced Pulmonary Arterial Hypertension
Hypertension 2009 53: 877-883.
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