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Protective Role of microRNA-200a in Diabetic Retinopathy Through Downregulation of PDLIM1
BACKGROUND: Diabetic retinopathy (DR) is a most common microvascular complication and regarded as the leading cause of blindness in the working age population. The involvement of miR-200a in various disorders has become recognized, and the objective of this study was to identify the protective effec...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8187036/ https://www.ncbi.nlm.nih.gov/pubmed/34113148 http://dx.doi.org/10.2147/JIR.S303540 |
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author | Wan, Wencui Long, Yang Jin, Xuemin Li, Qiuming Wan, Weiwei Liu, Hongzhuo Zhu, Yu |
author_facet | Wan, Wencui Long, Yang Jin, Xuemin Li, Qiuming Wan, Weiwei Liu, Hongzhuo Zhu, Yu |
author_sort | Wan, Wencui |
collection | PubMed |
description | BACKGROUND: Diabetic retinopathy (DR) is a most common microvascular complication and regarded as the leading cause of blindness in the working age population. The involvement of miR-200a in various disorders has become recognized, and the objective of this study was to identify the protective effect of miR-200a in the development of DR. METHODS: The contents of miR-200a and its potential target gene, PDZ and LIM domain protein 1 (PDLIM1), were detected in both in-vivo and in-vitro DR models. Retinal leakage and inflammatory factor concentrations were detected after vitreous injections of miR-200a/PDLIM1 vectors in mice. The cellular viability, apoptosis and cellular migration were investigated using trypan blue staining, flow cytometry and transwell assay with human retinal microvascular endothelial cells (HRMECs). Besides, the prediction and confirmation of miR-200a targeting PDLIM1 were conducted with bioinformation analyses and dual-luciferase reporter assay. RESULTS: Lower miR-200a and higher PDLIM1 levels were detected in both in-vivo and in-vitro DR models. Besides, it was found that miR-200a treatment would significantly inhibit retinal permeability and inflammatory factors. Through targeting PDLIM1, it was found that miR-200a could improve cellular viability, remit apoptotic status and reduce cellular migration significantly in high glucose-treated HRMECs. CONCLUSION: Our results demonstrated that miR-200a could be used as a potential therapy target through down-regulating PDLIM1 in DR. |
format | Online Article Text |
id | pubmed-8187036 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-81870362021-06-09 Protective Role of microRNA-200a in Diabetic Retinopathy Through Downregulation of PDLIM1 Wan, Wencui Long, Yang Jin, Xuemin Li, Qiuming Wan, Weiwei Liu, Hongzhuo Zhu, Yu J Inflamm Res Original Research BACKGROUND: Diabetic retinopathy (DR) is a most common microvascular complication and regarded as the leading cause of blindness in the working age population. The involvement of miR-200a in various disorders has become recognized, and the objective of this study was to identify the protective effect of miR-200a in the development of DR. METHODS: The contents of miR-200a and its potential target gene, PDZ and LIM domain protein 1 (PDLIM1), were detected in both in-vivo and in-vitro DR models. Retinal leakage and inflammatory factor concentrations were detected after vitreous injections of miR-200a/PDLIM1 vectors in mice. The cellular viability, apoptosis and cellular migration were investigated using trypan blue staining, flow cytometry and transwell assay with human retinal microvascular endothelial cells (HRMECs). Besides, the prediction and confirmation of miR-200a targeting PDLIM1 were conducted with bioinformation analyses and dual-luciferase reporter assay. RESULTS: Lower miR-200a and higher PDLIM1 levels were detected in both in-vivo and in-vitro DR models. Besides, it was found that miR-200a treatment would significantly inhibit retinal permeability and inflammatory factors. Through targeting PDLIM1, it was found that miR-200a could improve cellular viability, remit apoptotic status and reduce cellular migration significantly in high glucose-treated HRMECs. CONCLUSION: Our results demonstrated that miR-200a could be used as a potential therapy target through down-regulating PDLIM1 in DR. Dove 2021-06-04 /pmc/articles/PMC8187036/ /pubmed/34113148 http://dx.doi.org/10.2147/JIR.S303540 Text en © 2021 Wan et al. https://creativecommons.org/licenses/by-nc/3.0/This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/ (https://creativecommons.org/licenses/by-nc/3.0/) ). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Wan, Wencui Long, Yang Jin, Xuemin Li, Qiuming Wan, Weiwei Liu, Hongzhuo Zhu, Yu Protective Role of microRNA-200a in Diabetic Retinopathy Through Downregulation of PDLIM1 |
title | Protective Role of microRNA-200a in Diabetic Retinopathy Through Downregulation of PDLIM1 |
title_full | Protective Role of microRNA-200a in Diabetic Retinopathy Through Downregulation of PDLIM1 |
title_fullStr | Protective Role of microRNA-200a in Diabetic Retinopathy Through Downregulation of PDLIM1 |
title_full_unstemmed | Protective Role of microRNA-200a in Diabetic Retinopathy Through Downregulation of PDLIM1 |
title_short | Protective Role of microRNA-200a in Diabetic Retinopathy Through Downregulation of PDLIM1 |
title_sort | protective role of microrna-200a in diabetic retinopathy through downregulation of pdlim1 |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8187036/ https://www.ncbi.nlm.nih.gov/pubmed/34113148 http://dx.doi.org/10.2147/JIR.S303540 |
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