中国神经再生研究(英文版) ›› 2021, Vol. 16 ›› Issue (4): 621-627.doi: 10.4103/1673-5374.295271

• 综述:视神经损伤修复保护与再生 • 上一篇    下一篇

MicroRNAs在激光诱导小鼠和大鼠脉络膜新生血管中的表达及其潜在治疗靶点

  

  • 出版日期:2021-04-15 发布日期:2020-12-21

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

Bridget Martinez1, 2, Philip V. Peplow3, *   

  1. 1 Physical Chemistry and Applied Spectroscopy, Chemistry Division, Los Alamos National Laboratory, Los Alamos, NM, USA;  2 Department of Medicine, St. Georges University School of Medicine, Grenada;  3 Department of Anatomy, University of Otago, Dunedin, New Zealand
  • Online:2021-04-15 Published:2020-12-21
  • Contact: Philip V. Peplow, PhD, phil.peplow@otago.ac.nz.

摘要: https://orcid.org/0000-0001-5468-1989 (Philip V. Peplow) 

Abstract: 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, miR-24, miR-21, miR-31, miR-150, and miR-184, or suppression of miR-505, miR-126-3p, miR-155, 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.

Key words: age-related macular degeneration, angiogenesis, animal model, blood plasma, choroid, laser, microRNAs, neovascularization, retina, retinal pigment epithelium, therapeutic targets, vascular endothelial growth factor