Cargando…

The Role of Apelin/APJ in a Mouse Model of Oxygen-induced Retinopathy

PURPOSE: The aim of this study was to investigate apelin and its potential neovascularization role in retinopathy of prematurity (ROP) along with the inhibitory effects of its antagonist. METHODS: We used an oxygen-induced retinopathy (OIR) mouse model to explore the progress of ROP. Apelin and angi...

Descripción completa

Detalles Bibliográficos
Autores principales: Feng, Jing, Chen, Li, Jiang, Yanrong, Tao, Yong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Association for Research in Vision and Ophthalmology 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7425705/
https://www.ncbi.nlm.nih.gov/pubmed/32729912
http://dx.doi.org/10.1167/iovs.61.8.47
_version_ 1783570546217189376
author Feng, Jing
Chen, Li
Jiang, Yanrong
Tao, Yong
author_facet Feng, Jing
Chen, Li
Jiang, Yanrong
Tao, Yong
author_sort Feng, Jing
collection PubMed
description PURPOSE: The aim of this study was to investigate apelin and its potential neovascularization role in retinopathy of prematurity (ROP) along with the inhibitory effects of its antagonist. METHODS: We used an oxygen-induced retinopathy (OIR) mouse model to explore the progress of ROP. Apelin and angiotensin receptor-like 1 APJ expressions were examined in the retina using immunohistochemistry, quantitative polymerase chain reaction, and Western blot analysis. Additionally, the retina was examined by whole-mount staining to evaluate the retinal vessel area, vessel density, capillary width, and the number and length of tip cells. The expression of the phosphorylated mTOR (p-mTOR), p-PI3K/Akt, and p-Erk signaling pathway was also evaluated using Western blot analysis. RESULTS: Apelin promoted the development of superficial and deep retinal blood vessels, especially for tip cells during the physical development of retinal vessels. Additionally, apelin stimulated the density of the peripheral retinal zone vessels in OIR mice. The apelin and APJ expression levels significantly increased for the OIR model during their hypoxic phase. Next, we found that apelin mRNA levels in the OIR mice peaked at six hours after return to ambient conditions at P12, whereas the APJ mRNA levels peaked later at P17. Furthermore, the expression of p-mTOR, p-Akt, and p-Erk were all up-regulated in OIR mice whereas F13A suppressed them instead. CONCLUSIONS: Our results suggest that apelin/APJ signaling pathway is a key factor for hypoxia-induced pathologic angiogenesis, which is a very promising new target for the treatment of ROP.
format Online
Article
Text
id pubmed-7425705
institution National Center for Biotechnology Information
language English
publishDate 2020
publisher The Association for Research in Vision and Ophthalmology
record_format MEDLINE/PubMed
spelling pubmed-74257052020-08-26 The Role of Apelin/APJ in a Mouse Model of Oxygen-induced Retinopathy Feng, Jing Chen, Li Jiang, Yanrong Tao, Yong Invest Ophthalmol Vis Sci Retina PURPOSE: The aim of this study was to investigate apelin and its potential neovascularization role in retinopathy of prematurity (ROP) along with the inhibitory effects of its antagonist. METHODS: We used an oxygen-induced retinopathy (OIR) mouse model to explore the progress of ROP. Apelin and angiotensin receptor-like 1 APJ expressions were examined in the retina using immunohistochemistry, quantitative polymerase chain reaction, and Western blot analysis. Additionally, the retina was examined by whole-mount staining to evaluate the retinal vessel area, vessel density, capillary width, and the number and length of tip cells. The expression of the phosphorylated mTOR (p-mTOR), p-PI3K/Akt, and p-Erk signaling pathway was also evaluated using Western blot analysis. RESULTS: Apelin promoted the development of superficial and deep retinal blood vessels, especially for tip cells during the physical development of retinal vessels. Additionally, apelin stimulated the density of the peripheral retinal zone vessels in OIR mice. The apelin and APJ expression levels significantly increased for the OIR model during their hypoxic phase. Next, we found that apelin mRNA levels in the OIR mice peaked at six hours after return to ambient conditions at P12, whereas the APJ mRNA levels peaked later at P17. Furthermore, the expression of p-mTOR, p-Akt, and p-Erk were all up-regulated in OIR mice whereas F13A suppressed them instead. CONCLUSIONS: Our results suggest that apelin/APJ signaling pathway is a key factor for hypoxia-induced pathologic angiogenesis, which is a very promising new target for the treatment of ROP. The Association for Research in Vision and Ophthalmology 2020-07-30 /pmc/articles/PMC7425705/ /pubmed/32729912 http://dx.doi.org/10.1167/iovs.61.8.47 Text en Copyright 2020 The Authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
spellingShingle Retina
Feng, Jing
Chen, Li
Jiang, Yanrong
Tao, Yong
The Role of Apelin/APJ in a Mouse Model of Oxygen-induced Retinopathy
title The Role of Apelin/APJ in a Mouse Model of Oxygen-induced Retinopathy
title_full The Role of Apelin/APJ in a Mouse Model of Oxygen-induced Retinopathy
title_fullStr The Role of Apelin/APJ in a Mouse Model of Oxygen-induced Retinopathy
title_full_unstemmed The Role of Apelin/APJ in a Mouse Model of Oxygen-induced Retinopathy
title_short The Role of Apelin/APJ in a Mouse Model of Oxygen-induced Retinopathy
title_sort role of apelin/apj in a mouse model of oxygen-induced retinopathy
topic Retina
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7425705/
https://www.ncbi.nlm.nih.gov/pubmed/32729912
http://dx.doi.org/10.1167/iovs.61.8.47
work_keys_str_mv AT fengjing theroleofapelinapjinamousemodelofoxygeninducedretinopathy
AT chenli theroleofapelinapjinamousemodelofoxygeninducedretinopathy
AT jiangyanrong theroleofapelinapjinamousemodelofoxygeninducedretinopathy
AT taoyong theroleofapelinapjinamousemodelofoxygeninducedretinopathy
AT fengjing roleofapelinapjinamousemodelofoxygeninducedretinopathy
AT chenli roleofapelinapjinamousemodelofoxygeninducedretinopathy
AT jiangyanrong roleofapelinapjinamousemodelofoxygeninducedretinopathy
AT taoyong roleofapelinapjinamousemodelofoxygeninducedretinopathy