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Abstracts 2023 год

Abstracts
статья из журнала

Полный текстСтраница публикацииПубликация в OpenAlex
Аннотация: Visual impairment affects over 314 million people world-wide.Currently, electrode-based prostheses are the most successful in restoring some forms of vision; however, they lack cell specific targeting and can harm the tissue.Optogenetics uses targeted ectopic expression of light-activated proteins (opsins) to control cell specific neural activity with millisecond precision, thus emerging as a promising therapy and does not present the flaws of electrode-based prostheses.Taking this into account, lLEDbased optogenetic prostheses could photostimulate tissues with cells expressing opsins.Viruses are commonly used to introduce the opsin genes in neurons; however, they can cause immunogenic reactions.Therefore, it is necessary to find safer alternatives.In this work, we aim to use niosomes and electroporation in central nervous system (CNS) cells to test the suitability of these non-viral vectors for photosensitizing them.Optogenetic plasmids pAAV-Syn-ChrimsonR-tdTomato and pCAG-Chrim-sonR-tdTomato (both coding for ChrimsonR protein, a red shifted opsin activated at 590 nm) were delivered in both in vitro and in vivo experiments.In vitro experiments in rat cortical neurons were performed with different formulations of niosomes that delivered the optogenetic plasmids, while the in vivo experiments were performed in a retinal degeneration mouse model (rd10) delivering the optogenetic plasmids into the retina by electroporation.Niosomes and electroporation have proven to effectively deliver optogenetic material into CNS cells, but niosome formulations affect both morphologically and electrophysiologically cortical neurons, while electroporation does not produce light-driven visual behavior in rd10 mice.However, non-viral vectors are varied and alternative ways for transfecting cells should be tested.
Год издания: 2023
Издательство: Wiley
Источник: FEBS Open Bio
Другие ссылки: FEBS Open Bio (PDF)
FEBS Open Bio (HTML)
PubMed Central (HTML)
PubMed (HTML)