当前位置： SCI文献检索 > BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS期刊下所有文献 > LincRNA TINCR facilitates excessive proliferation and inflammation in post-burn skin fibroblasts by directly binding with SND1 protein and inducing SND1-mediated TGF-β1 expression.

LincRNA TINCR facilitates excessive proliferation and inflammation in post-burn skin fibroblasts by directly binding with SND1 protein and inducing SND1-mediated TGF-β1 expression.

Abstract：

: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.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Qin G,Song Y,Guo Y,Sun Y,Zeng W

doi

10.1016/j.bbrc.2019.01.013

subject

Has Abstract

pub_date

2019-02-19 00:00:00

pages

903-910

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(19)30019-1

journal_volume

509

pub_type

杂志文章

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