Effects of Apelin on the fibrosis of retinal tissues and Müller cells in diabetes retinopathy through the JAK2/STAT3 signalling pathway

Retinal fibrosis was a key characteristic of diabetes retinopathy (DR). Apelin was found to be a candidate for tissue fibrosis. Nevertheless, the role of Apelin in the Müller cells in DR remains unclear. This study identified the function and mechanism of Apelin in Müller cells and the fibrosis of r...

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Main Authors: Yang Li, Qinrui Hu, Bin Wang
Format: Article
Language:English
Published: Taylor & Francis Group 2023-12-01
Series:Autoimmunity
Subjects:
Online Access:http://dx.doi.org/10.1080/08916934.2023.2259129
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author Yang Li
Qinrui Hu
Bin Wang
author_facet Yang Li
Qinrui Hu
Bin Wang
author_sort Yang Li
collection DOAJ
description Retinal fibrosis was a key characteristic of diabetes retinopathy (DR). Apelin was found to be a candidate for tissue fibrosis. Nevertheless, the role of Apelin in the Müller cells in DR remains unclear. This study identified the function and mechanism of Apelin in Müller cells and the fibrosis of retinal tissue. Western blot was carried out to detect the Apelin, GFAP, Collagen I, α-SMA, JAK2 and STAT3 protein levels. Masson staining was performed to display the histopathological changes in retinal tissue of diabetic mellitus (DM) rats. The immunofluorescence staining was conducted to evaluate the Apelin levels in the retinal tissue. The levels of GFAP, Collagen I and α-SMA in the retinal tissue of DM rats was visualised by the immunohistochemistry staining. The results showed that Apelin, GFAP, Collagen I andα-SMA expression was prominently elevated in the retinal tissue of DM rats and high glucose (HG)-exposed Müller cells. The results of Masson staining showed that the epiretinal fibrotic membrane was observed in DM rats. Apelin knockdown declined the GFAP, Collagen I andα-SMA levels. Besides, the protein levels of p-JAK2 and p-STAT3 were elevated in the HG-treated Müller cells, while Apelin knockdown declined them. FLLL32 treatment neutralised the role of Apelin. In conclusion, Apelin facilitated the fibrogenic activity of Müller cells through activating the JAK2/STAT3 signalling pathway, and thus inducing the retinal fibrosis in DR.
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spelling doaj.art-cb6fdeeff5c641a1887d03abe73730012023-11-03T16:27:52ZengTaylor & Francis GroupAutoimmunity0891-69341607-842X2023-12-0156110.1080/08916934.2023.22591292259129Effects of Apelin on the fibrosis of retinal tissues and Müller cells in diabetes retinopathy through the JAK2/STAT3 signalling pathwayYang Li0Qinrui Hu1Bin Wang2Xiamen Eye Center, Xiamen UniversityXiamen Eye Center, Xiamen UniversityXiamen Eye Center, Xiamen UniversityRetinal fibrosis was a key characteristic of diabetes retinopathy (DR). Apelin was found to be a candidate for tissue fibrosis. Nevertheless, the role of Apelin in the Müller cells in DR remains unclear. This study identified the function and mechanism of Apelin in Müller cells and the fibrosis of retinal tissue. Western blot was carried out to detect the Apelin, GFAP, Collagen I, α-SMA, JAK2 and STAT3 protein levels. Masson staining was performed to display the histopathological changes in retinal tissue of diabetic mellitus (DM) rats. The immunofluorescence staining was conducted to evaluate the Apelin levels in the retinal tissue. The levels of GFAP, Collagen I and α-SMA in the retinal tissue of DM rats was visualised by the immunohistochemistry staining. The results showed that Apelin, GFAP, Collagen I andα-SMA expression was prominently elevated in the retinal tissue of DM rats and high glucose (HG)-exposed Müller cells. The results of Masson staining showed that the epiretinal fibrotic membrane was observed in DM rats. Apelin knockdown declined the GFAP, Collagen I andα-SMA levels. Besides, the protein levels of p-JAK2 and p-STAT3 were elevated in the HG-treated Müller cells, while Apelin knockdown declined them. FLLL32 treatment neutralised the role of Apelin. In conclusion, Apelin facilitated the fibrogenic activity of Müller cells through activating the JAK2/STAT3 signalling pathway, and thus inducing the retinal fibrosis in DR.http://dx.doi.org/10.1080/08916934.2023.2259129apelinmüller cellsfibrosisdiabetes retinopathyjak2/stat3
spellingShingle Yang Li
Qinrui Hu
Bin Wang
Effects of Apelin on the fibrosis of retinal tissues and Müller cells in diabetes retinopathy through the JAK2/STAT3 signalling pathway
Autoimmunity
apelin
müller cells
fibrosis
diabetes retinopathy
jak2/stat3
title Effects of Apelin on the fibrosis of retinal tissues and Müller cells in diabetes retinopathy through the JAK2/STAT3 signalling pathway
title_full Effects of Apelin on the fibrosis of retinal tissues and Müller cells in diabetes retinopathy through the JAK2/STAT3 signalling pathway
title_fullStr Effects of Apelin on the fibrosis of retinal tissues and Müller cells in diabetes retinopathy through the JAK2/STAT3 signalling pathway
title_full_unstemmed Effects of Apelin on the fibrosis of retinal tissues and Müller cells in diabetes retinopathy through the JAK2/STAT3 signalling pathway
title_short Effects of Apelin on the fibrosis of retinal tissues and Müller cells in diabetes retinopathy through the JAK2/STAT3 signalling pathway
title_sort effects of apelin on the fibrosis of retinal tissues and muller cells in diabetes retinopathy through the jak2 stat3 signalling pathway
topic apelin
müller cells
fibrosis
diabetes retinopathy
jak2/stat3
url http://dx.doi.org/10.1080/08916934.2023.2259129
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AT qinruihu effectsofapelinonthefibrosisofretinaltissuesandmullercellsindiabetesretinopathythroughthejak2stat3signallingpathway
AT binwang effectsofapelinonthefibrosisofretinaltissuesandmullercellsindiabetesretinopathythroughthejak2stat3signallingpathway