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aging-v12i24-202404.pdf
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Author
Ménard, C.Wilson, A.M.
Dejda, A.
Miloudi, K.
Binet, F.
Crespo-Garcia, S.
Parinot, C.
Pilon, F.
Juneau, R.
Andriessen, E.M.
Mawambo, G.
SanGiovanni, J.P.
Guire, V.D.
Sapieha, P.
Affiliation
Department of Nutritional Sciences, University of ArizonaIssue Date
2020
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Impact Journals LLCCitation
Ménard, C., Wilson, A. M., Dejda, A., Miloudi, K., Binet, F., Crespo-Garcia, S., ... & Sapieha, P. (2020). miR-106b suppresses pathological retinal angiogenesis. Aging (Albany NY), 12(24), 24836.Journal
AgingRights
Copyright © 2020 Ménard et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0).Collection Information
This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.Abstract
MicroRNAs are small non-coding RNAs that post-transcriptionally regulate gene expression. We recently demonstrated that levels of miR-106b were significantly decreased in the vitreous and plasma of patients with neovascular age-related macular degeneration (AMD). Here we show that expression of the miR-106b-25 cluster is negatively regulated by the unfolded protein response pathway of protein kinase RNA-like ER kinase (PERK) in a mouse model of neovascular AMD. A reduction in levels of miR-106b triggers vascular growth both in vivo and in vitro by inducing production of pro-angiogenic factors. We demonstrate that therapeutic delivery of miR-106b to the retina with lentiviral vectors protects against aberrant retinal angiogenesis in two distinct mouse models of pathological retinal neovascularization. Results from this study suggest that miRNAs such as miR-106b have the potential to be used as multitarget therapeutics for conditions characterized by pathological retinal angiogenesis. © 2020 Ménard et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.Note
Open access journalISSN
1945-4589Version
Final published versionae974a485f413a2113503eed53cd6c53
10.18632/aging.202404
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Except where otherwise noted, this item's license is described as Copyright © 2020 Ménard et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0).