MicroRNAs in laser-induced choroidal neovascularization in mice and rats: their expression and potential therapeutic targets

Journal Article · Fri Oct 09 00:00:00 EDT 2020 · Neural Regeneration Research

DOI:https://doi.org/10.4103/1673-5374.295271· OSTI ID:1815808

Martinez, Bridget ^[1]; Peplow, Philip V. ^[2]

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1. Los Alamos National Lab. (LANL), Los Alamos, NM (United States). Chemistry Division. Physical Chemistry and Applied Spectroscopy; St. Georges Univ. (Grenada). School of Medicine. Dept. of Medicine; OSTI
2. Univ. of Otago, Dunedin (New Zealand). Dept. of Anatomy

Choroidal neovascularization characterizes wet age-related macular degeneration. Choroidal neovascularization formation involves a primarily angiogenic process that is combined with both inflammation and proteolysis. A primary cause of choroidal neovascularization pathogenesis is alterations in pro- and anti-angiogenic factors derived from the retinal pigment epithelium, with vascular endothelium growth factor being mainly responsible for both clinical and experimental choroidal neovascularization. MicroRNAs (miRNAs) which are short, non-coding, endogenous RNA molecules have a major role in regulating various pathological processes, including inflammation and angiogenesis. A review of recent studies with the mouse laser-induced choroidal neovascularization model has shown alterations in miRNA expression in choroidal neovascularization tissues and could be potential therapeutic targets for wet age-related macular degeneration. Upregulation of miR-505 (days 1 and 3 post-laser), miR-155 (day 14) occurred in retina; miR-342-5p (days 3 and 7), miR-126-3p (day 14) in choroid; miR-23a, miR-24, miR-27a (day 7) in retina/choroid; miR-505 (days 1 and 3) in retinal pigment epithelium/choroid; downregulation of miR-155 (days 1 and 3), miR-29a, miR-29b, miR-29c (day 5), miR-93 (day 14), miR-126 (day 14) occurred in retinal pigment epithelium/choroid. Therapies using miRNA mimics or inhibitors were found to decrease choroidal neovascularization lesions. Choroidal neovascularization development was reduced by overexpression of miR-155, miR-188-5p, miR-(5,B,7), miR-126-3p, miR-342-5p, miR-93, miR-126, miR-195a-3p, miR24, miR-21, miR-31, miR-150, and miR-184, or suppression of miR-505, miR-126-3p, miR155, and miR-23/27. Further studies are warranted to determine miRNA expression in mouse laser-induced choroidal neovascularization models in order to validate and extend the reported findings. Important experimental variables need to be standardized; these include the strain and age of animals, gender, number and position of laser burns to the eye, laser parameters to induce choroidal neovascularization lesions including wavelength, power, spot size, and duration.

• Sponsoring Organization: USDOE National Nuclear Security Administration (NNSA)
• Grant/Contract Number: 89233218CNA000001
• OSTI ID: 1815808
• Journal Information: Neural Regeneration Research, Journal Name: Neural Regeneration Research Journal Issue: 4 Vol. 16; ISSN 1673-5374
• Publisher: Chinese Association of Rehabilitation Medicine (CARM)
• Country of Publication: United States
• Language: English

Related Subjects

therapeutic targets
59 BASIC BIOLOGICAL SCIENCES
60 APPLIED LIFE SCIENCES
age-related macular degeneration
angiogenesis
animal model
blood plasma
choroid
laser
microRNAs
neovascularization
retina
retinal pigment epithelium
vascular endothelial growth factor