Premium
miR‐140‐5p‐mediated regulation of the proliferation and differentiation of human dental pulp stem cells occurs through the lipopolysaccharide/toll‐like receptor 4 signaling pathway
Author(s) -
Sun Degang,
Xin Bingchang,
Wu Di,
Zhou Lei,
Wu Hongbin,
Gong Wen,
Lv Jian
Publication year - 2017
Publication title -
european journal of oral sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.802
H-Index - 93
eISSN - 1600-0722
pISSN - 0909-8836
DOI - 10.1111/eos.12384
Subject(s) - dental pulp stem cells , microbiology and biotechnology , microrna , toll like receptor , stem cell , tlr4 , cellular differentiation , mesenchymal stem cell , biology , cell growth , signal transduction , receptor , chemistry , innate immune system , gene , genetics
Human dental pulp stem cells ( DPSC s) are oral mesenchymal stem cells with potential to differentiate into various cell types. Recent studies of DPSC s have focused on micro RNA s (mi RNA s), a class of small noncoding RNA s that play crucial roles in regulating DPSC phenotypes. In the current study, the expression of miR‐140‐5p was significantly decreased during lipopolysaccharide ( LPS )‐mediated differentiation of DPSC s in vitro. Overexpression of miR‐140‐5p enhanced proliferation of DPSC s and inhibited DPSC differentiation, whereas suppression of miR‐140‐5p produced the opposite effect. Moreover, the expression of toll‐like receptor 4 ( TLR ‐4), a critical regulator of DPSC s, was negatively correlated with the levels of miR‐140‐5p. A luciferase reporter analysis confirmed that miR‐140‐5p could regulate TLR ‐4 by directly binding to the 3′‐untranslated region (3′‐ UTR ) of the TLR 4 mRNA . Additionally, we suppressed TLR ‐4 expression by treating cells with a TLR ‐4 inhibitor, CLI ‐095, and demonstrated that the effect of the miR‐140‐5p inhibitor on DPSC proliferation and differentiation could be partially reversed by blocking TLR ‐4. Taken together, our data suggest that miR‐140‐5p is a novel mi RNA that regulates DPSC proliferation and differentiation.