Please use this identifier to cite or link to this item: http://lib.jncasr.ac.in:8080/jspui/handle/10572/140
Title: Intrinsically Fluorescent Carbon Nanospheres as a Nuclear Targeting Vector: Delivery of Membrane-Impermeable Molecule to Modulate Gene Expression In Vivo
Authors: Selvi, B R
Jagadeesan, D
Suma, B S
Nagashankar, G
Arif, M
Balasubramanyam, K
Eswaramoorthy, M
Kundu, Tapas K
Keywords: Blood-Brain-Barrier
Drug-Delivery
Cells
Nanoparticles
Nanotubes
Chromatin
Transporters
Transcription
System
Particles
Issue Date: 1-Oct-2008
Publisher: American Chemical Society
Citation: Nano Letters 8(10), 3182-3188 (2008)
Abstract: In this report, we demonstrate glucose-derived carbon nanospheres(1) to be an emerging class of intracellular carriers. The surfaces of these spheres are highly functionalized and do not need any further modification. Besides, the intrinsic fluorescence property of carbon nanospheres helps in tracking their cellular localization without any additional fluorescent tags. The spheres are found to target the nucleus of the mammalian cells, causing no toxicity. Interestingly, the in vivo experiments show that these nanospheres have an important ability to cross the blood-brain barrier and localize in the brain besides getting localized in the liver and the spleen. There is also evidence to show that they are continuously being removed from these tissues over time. Furthermore, these nanospheres were used as a carrier for the membrane-impermeable molecule CTPB (N-(4-chloro-3-trifluoromethylphenyl)-2-ethoxybenzamide), the only known small-molecule activator of histone acetyltransferase (HAT) p300.(2) Biochemical analyses such as Western blotting, immunohistochemistry, and gene expression analysis show the induction of the hyperacetylation of histone acetyltransferase (HAT) p300 (autoacetylation) as well as histones both in vitro and in vivo and the activation of HAT-dependent transcription upon CTPB delivery. These results establish an alternative path for the activation of gene expression mediated by the induction of HAT activity instead of histone deacetylase (HDAC) inhibition.
URI: http://hdl.handle.net/10572/140
Other Identifiers: 1530-6984
Appears in Collections:Research Papers (Tapas K. Kundu)

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