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The Effect of STAT3 Signal Pathway Activation on Retinopathy of Prematurity

Objective: To investigate the mechanism of activation of the signal transducer and activator of transcription 3 (STAT3) signal pathway in the process of retinopathy of prematurity (ROP). Methods: Sixty newborn Sprague-Dawley (SD) rats were randomly separated into the hyperoxia and air control groups...

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Autores principales: Ren, Jianbing, Jiang, Jingbo, Ou, Weiming, Luo, Xianqiong, Xiang, Jianwen, Liu, Guosheng, Huang, Shuiqing, He, Longkai, Gan, Jiamin, Li, Hongping, Nie, Chuan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8631452/
https://www.ncbi.nlm.nih.gov/pubmed/34858895
http://dx.doi.org/10.3389/fped.2021.638432
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author Ren, Jianbing
Jiang, Jingbo
Ou, Weiming
Luo, Xianqiong
Xiang, Jianwen
Liu, Guosheng
Huang, Shuiqing
He, Longkai
Gan, Jiamin
Li, Hongping
Nie, Chuan
author_facet Ren, Jianbing
Jiang, Jingbo
Ou, Weiming
Luo, Xianqiong
Xiang, Jianwen
Liu, Guosheng
Huang, Shuiqing
He, Longkai
Gan, Jiamin
Li, Hongping
Nie, Chuan
author_sort Ren, Jianbing
collection PubMed
description Objective: To investigate the mechanism of activation of the signal transducer and activator of transcription 3 (STAT3) signal pathway in the process of retinopathy of prematurity (ROP). Methods: Sixty newborn Sprague-Dawley (SD) rats were randomly separated into the hyperoxia and air control groups (n = 30/in each group). The serum hepcidin level on 21 d was measured using the enzyme-linked immunosorbent assay (ELISA). The expression of HAMP and STAT3 protein in the liver was determined using reverse transcription-polymerase chain reaction (RT-PCR) and western blotting. Retinal neovasculature was evaluated by hematoxylin and eosin (HE) stain and fluorescein lectin. The retinal endothelial cells were treated with 250 μmol/L cobalt chloride for 72 h and added S3I-201. The STAT3 level was determined by western blotting. Results: The expression of STAT3 protein increased significantly after hyperoxia stimulation. The expression of HAMP mRNA in the hyperoxia group was significantly higher than that of the control group. The proliferation of retinal cells was inhibited, and the expression of STAT3 was increased. No significant difference was noted in vascular endothelial growth factor (VEGF) mRNA. The expression of STAT3 and VEGF mRNA was significantly reduced. Conclusion: The activation of the STAT3 signal pathway increased hepcidin expression, contributing to the pathogenesis of ROP. S3I-201 inhibited the expression of STAT3 and VEGF mRNA levels. This information provides potential novel therapeutic approach to the prevention and treatment of ROP.
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spelling pubmed-86314522021-12-01 The Effect of STAT3 Signal Pathway Activation on Retinopathy of Prematurity Ren, Jianbing Jiang, Jingbo Ou, Weiming Luo, Xianqiong Xiang, Jianwen Liu, Guosheng Huang, Shuiqing He, Longkai Gan, Jiamin Li, Hongping Nie, Chuan Front Pediatr Pediatrics Objective: To investigate the mechanism of activation of the signal transducer and activator of transcription 3 (STAT3) signal pathway in the process of retinopathy of prematurity (ROP). Methods: Sixty newborn Sprague-Dawley (SD) rats were randomly separated into the hyperoxia and air control groups (n = 30/in each group). The serum hepcidin level on 21 d was measured using the enzyme-linked immunosorbent assay (ELISA). The expression of HAMP and STAT3 protein in the liver was determined using reverse transcription-polymerase chain reaction (RT-PCR) and western blotting. Retinal neovasculature was evaluated by hematoxylin and eosin (HE) stain and fluorescein lectin. The retinal endothelial cells were treated with 250 μmol/L cobalt chloride for 72 h and added S3I-201. The STAT3 level was determined by western blotting. Results: The expression of STAT3 protein increased significantly after hyperoxia stimulation. The expression of HAMP mRNA in the hyperoxia group was significantly higher than that of the control group. The proliferation of retinal cells was inhibited, and the expression of STAT3 was increased. No significant difference was noted in vascular endothelial growth factor (VEGF) mRNA. The expression of STAT3 and VEGF mRNA was significantly reduced. Conclusion: The activation of the STAT3 signal pathway increased hepcidin expression, contributing to the pathogenesis of ROP. S3I-201 inhibited the expression of STAT3 and VEGF mRNA levels. This information provides potential novel therapeutic approach to the prevention and treatment of ROP. Frontiers Media S.A. 2021-11-10 /pmc/articles/PMC8631452/ /pubmed/34858895 http://dx.doi.org/10.3389/fped.2021.638432 Text en Copyright © 2021 Ren, Jiang, Ou, Luo, Xiang, Liu, Huang, He, Gan, Li and Nie. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Pediatrics
Ren, Jianbing
Jiang, Jingbo
Ou, Weiming
Luo, Xianqiong
Xiang, Jianwen
Liu, Guosheng
Huang, Shuiqing
He, Longkai
Gan, Jiamin
Li, Hongping
Nie, Chuan
The Effect of STAT3 Signal Pathway Activation on Retinopathy of Prematurity
title The Effect of STAT3 Signal Pathway Activation on Retinopathy of Prematurity
title_full The Effect of STAT3 Signal Pathway Activation on Retinopathy of Prematurity
title_fullStr The Effect of STAT3 Signal Pathway Activation on Retinopathy of Prematurity
title_full_unstemmed The Effect of STAT3 Signal Pathway Activation on Retinopathy of Prematurity
title_short The Effect of STAT3 Signal Pathway Activation on Retinopathy of Prematurity
title_sort effect of stat3 signal pathway activation on retinopathy of prematurity
topic Pediatrics
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8631452/
https://www.ncbi.nlm.nih.gov/pubmed/34858895
http://dx.doi.org/10.3389/fped.2021.638432
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