Open AccessThe Long Noncoding RNA LINC00963 Inhibits Corneal Fibrosis Scar Formation by Targeting miR-143-3p
Author(s) -
Lixia Zhang,
Jinling Gao,
Anjing Gong,
Yanhan Dong,
Xiaodan Hao,
Xuekang Wang,
Jian Zheng,
Wenmeng Ma,
Yiying Song,
Jie Zhang,
Wu Xu
Publication year - 2022
Publication title -
dna and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.895
H-Index - 77
eISSN - 1557-7430
pISSN - 1044-5498
DOI - 10.1089/dna.2021.1034
Subject(s) - myofibroblast , stromal cell , fibrosis , biology , downregulation and upregulation , transforming growth factor , western blot , smad , stroma , cornea , cancer research , blot , microbiology and biotechnology , pathology , immunology , medicine , immunohistochemistry , gene , biochemistry , neuroscience
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.