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

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Tác giả:

Ngôn ngữ: eng

Ký hiệu phân loại: 591.7 Animal ecology, animals characteristic of specific environments

Thông tin xuất bản: Washington, D.C. : Oak Ridge, Tenn. : United States. National Nuclear Security Administration ; Distributed by the Office of Scientific and Technical Information, U.S. Dept. of Energy, 2020

Mô tả vật lý: Size: p. 621-627 : , digital, PDF file.

Bộ sưu tập: Metadata

ID: 261766

 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.
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