Role of the long noncoding RNA H19 in TGF- β1-induced Tenon's capsule fibroblast proliferation and extracellular matrix deposition.

In this study, we first isolated primary human Tenon's capsule fibroblasts (HTFs) and found that TGF-β promoted the viability, proliferation and extracellular matrix (ECM) deposition of HTFs. Then, we showed that TGF-β promoted the expression of H19 in HTFs and that suppression of H19 inhibited the effect of TGF-β on HTFs. Furthermore, we revealed that H19 exerted its effects by interacting with miR-200a in TGF-β-treated HTFs. Additionally, we showed that β-catenin was a target of miR-200a in TGF-β-treated HTFs. We also demonstrated that H19 acted by modulating the H19/miR-200a/β-catenin regulatory axis in TGF-β-treated HTFs. Ultimately, we found that the components of the H19/miR-200a/β-catenin regulatory axis were aberrantly expressed in a rat model of GFS. Our results show that H19 indeed acts by modulating β-catenin expression via miR-200a in TGF-β-treated HTFs, thus providing a novel rationale for the development of H19-based strategies to attenuate scar formation after GFS. PMID: 31877306 [PubMed - as supplied by publisher]
Source: Experimental Cell Research - Category: Cytology Authors: Tags: Exp Cell Res Source Type: research