In this study, we found that lincRNA-TINCR was significantly upregulated in burn-injured skin tissues in vivo and heat-stimulated dermal fibroblasts in vitro, accompanied by an increase in TGF-β1 expression. TINCR overexpression promoted cell proliferation, colony formation, release of pro-inflammatory factors and expression of TGF-β1 protein in human primary fibroblasts under normal condition. Moreover, silencing TINCR reduced expression of TGF-β1, cell proliferation, colony formation and inflammation in heat-stressed fibroblasts. Subsequently, motif analysis in TINCR sequence revealed that there were two potential target sites for the RNA-binding protein Staphylococcal Nuclease and Tudor Domain Containin... More
In this study, we found that lincRNA-TINCR was significantly upregulated in burn-injured skin tissues in vivo and heat-stimulated dermal fibroblasts in vitro, accompanied by an increase in TGF-β1 expression. TINCR overexpression promoted cell proliferation, colony formation, release of pro-inflammatory factors and expression of TGF-β1 protein in human primary fibroblasts under normal condition. Moreover, silencing TINCR reduced expression of TGF-β1, cell proliferation, colony formation and inflammation in heat-stressed fibroblasts. Subsequently, motif analysis in TINCR sequence revealed that there were two potential target sites for the RNA-binding protein Staphylococcal Nuclease and Tudor Domain Containing 1 (SND1). We verified their direct binding by using RNA-IP assays using wild-type or mutated biotinylated TINCR transcripts TINCR and demonstrated that TINCR overexpression enhanced the binding of TINCR and SND1. Furthermore, SND1 knockdown improved fibroblast behaviors, like silencing TINCR, and SND1 overexpression could antagonize the effect of silencing TINCR on fibroblast proliferation and inflammation.,Copyright © 2019 Elsevier Inc. All rights reserved.
