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The Long Noncoding RNA LINC00963 Inhibits Corneal Fibrosis Scar Formation by Targeting miR-143-3p
Corneal fibrosis is a complication of severe corneal injury, one of the major causes of vision loss. The formation of myofibroblasts has emerged as a key stimulative factor of corneal fibrosis. In the current study, we focused on the role of LINC00963 in regulating corneal fibrosis. Transforming gro...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Mary Ann Liebert, Inc., publishers
2022
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9063159/ https://www.ncbi.nlm.nih.gov/pubmed/35262384 http://dx.doi.org/10.1089/dna.2021.1034 |
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author | Zhang, Lixia Gao, Jinning Gong, Anjing Dong, Yanhan Hao, Xiaodan Wang, Xuekang Zheng, Jian Ma, Wenmeng Song, Yiying Zhang, Jie Xu, Wenhua |
author_facet | Zhang, Lixia Gao, Jinning Gong, Anjing Dong, Yanhan Hao, Xiaodan Wang, Xuekang Zheng, Jian Ma, Wenmeng Song, Yiying Zhang, Jie Xu, Wenhua |
author_sort | Zhang, Lixia |
collection | PubMed |
description | Corneal fibrosis is a complication of severe corneal injury, one of the major causes of vision loss. The formation of myofibroblasts has emerged as a key stimulative factor of corneal fibrosis. In the current study, we focused on the role of LINC00963 in regulating corneal fibrosis. Transforming growth factor β1 (TGF-β1) was used to induce human corneal stromal cells differentiating into corneal myofibroblasts, and the significant increase of α-smooth muscle actin (α-SMA) was verified by quantitative real-time PCR (qRT-PCR), western blot, and immunofluorescence, respectively. LINC00963 was identified to be one-half decreased compared with nonstimulated human corneal stromal cells, indicating that it might play a role in corneal fibrosis. Interestingly, overexpression of LINC00963 resulted in decreased formation of myofibroblasts indicating that it might exhibit an inhibiting effect. Moreover, bioinformatics tool was applied to predict the downstream target of LINC00963. We investigated that LINC00963 suppressed α-SMA induced by TGF-β1 in corneal fibroblasts, at least in part, by downregulating the expression of miR-143-3p. In addition, either LINC00963 promotion or miR-143-3p inhibition could significantly decrease myofibroblast contractility and collagen I and III secretion, which are the key to contribute to corneal fibrosis. Taken together, our study identified LINC00963 as a promising therapeutic target. |
format | Online Article Text |
id | pubmed-9063159 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Mary Ann Liebert, Inc., publishers |
record_format | MEDLINE/PubMed |
spelling | pubmed-90631592022-05-03 The Long Noncoding RNA LINC00963 Inhibits Corneal Fibrosis Scar Formation by Targeting miR-143-3p Zhang, Lixia Gao, Jinning Gong, Anjing Dong, Yanhan Hao, Xiaodan Wang, Xuekang Zheng, Jian Ma, Wenmeng Song, Yiying Zhang, Jie Xu, Wenhua DNA Cell Biol RNA Corneal fibrosis is a complication of severe corneal injury, one of the major causes of vision loss. The formation of myofibroblasts has emerged as a key stimulative factor of corneal fibrosis. In the current study, we focused on the role of LINC00963 in regulating corneal fibrosis. Transforming growth factor β1 (TGF-β1) was used to induce human corneal stromal cells differentiating into corneal myofibroblasts, and the significant increase of α-smooth muscle actin (α-SMA) was verified by quantitative real-time PCR (qRT-PCR), western blot, and immunofluorescence, respectively. LINC00963 was identified to be one-half decreased compared with nonstimulated human corneal stromal cells, indicating that it might play a role in corneal fibrosis. Interestingly, overexpression of LINC00963 resulted in decreased formation of myofibroblasts indicating that it might exhibit an inhibiting effect. Moreover, bioinformatics tool was applied to predict the downstream target of LINC00963. We investigated that LINC00963 suppressed α-SMA induced by TGF-β1 in corneal fibroblasts, at least in part, by downregulating the expression of miR-143-3p. In addition, either LINC00963 promotion or miR-143-3p inhibition could significantly decrease myofibroblast contractility and collagen I and III secretion, which are the key to contribute to corneal fibrosis. Taken together, our study identified LINC00963 as a promising therapeutic target. Mary Ann Liebert, Inc., publishers 2022-04-01 2022-04-19 /pmc/articles/PMC9063159/ /pubmed/35262384 http://dx.doi.org/10.1089/dna.2021.1034 Text en © Lixia Zhang et al. 2022; Published by Mary Ann Liebert, Inc. https://creativecommons.org/licenses/by/4.0/This Open Access article is distributed under the terms of the Creative Commons License [CC-BY] (http://creativecommons.org/licenses/by/4.0 (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | RNA Zhang, Lixia Gao, Jinning Gong, Anjing Dong, Yanhan Hao, Xiaodan Wang, Xuekang Zheng, Jian Ma, Wenmeng Song, Yiying Zhang, Jie Xu, Wenhua The Long Noncoding RNA LINC00963 Inhibits Corneal Fibrosis Scar Formation by Targeting miR-143-3p |
title | The Long Noncoding RNA LINC00963 Inhibits Corneal Fibrosis Scar Formation by Targeting miR-143-3p |
title_full | The Long Noncoding RNA LINC00963 Inhibits Corneal Fibrosis Scar Formation by Targeting miR-143-3p |
title_fullStr | The Long Noncoding RNA LINC00963 Inhibits Corneal Fibrosis Scar Formation by Targeting miR-143-3p |
title_full_unstemmed | The Long Noncoding RNA LINC00963 Inhibits Corneal Fibrosis Scar Formation by Targeting miR-143-3p |
title_short | The Long Noncoding RNA LINC00963 Inhibits Corneal Fibrosis Scar Formation by Targeting miR-143-3p |
title_sort | long noncoding rna linc00963 inhibits corneal fibrosis scar formation by targeting mir-143-3p |
topic | RNA |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9063159/ https://www.ncbi.nlm.nih.gov/pubmed/35262384 http://dx.doi.org/10.1089/dna.2021.1034 |
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