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 growth factor beta 1 (TGF-beta 1) was used to induce human corneal stromal cells differentiating into corneal myofibroblasts, and the significant increase of alpha-smooth muscle actin (alpha-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 alpha-SMA induced by TGF-beta 1 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.

Automated summary

The study explored the role of LINC00963 in regulating corneal fibrosis, finding that its overexpression can inhibit the formation of myofibroblasts and affect the contractility and secretion of collagen I and III in corneal fibroblasts by downregulating miR-143-3p expression. The research suggests LINC00963 as a promising therapeutic target for corneal fibrosis.