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Micro RNA ‐135b inhibits odontoblast‐like differentiation of human dental pulp cells by regulating Smad5 and Smad4
Author(s) -
Song Z.,
Chen L. L.,
Wang R. F.,
Qin W.,
Huang S. H.,
Guo J.,
Lin Z. M.,
Tian Y. G.
Publication year - 2017
Publication title -
international endodontic journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.988
H-Index - 119
eISSN - 1365-2591
pISSN - 0143-2885
DOI - 10.1111/iej.12678
Subject(s) - odontoblast , microrna , microbiology and biotechnology , cellular differentiation , chemistry , pulp (tooth) , biology , dentistry , gene , medicine , biochemistry
Aim To investigate the function of mi RNA s in odontoblast‐like differentiation of human dental pulp cells (hDPCs). Methodology Integrated comparative mi RNA microarray profiling was used to determine the differential mi RNA s expression in odontoblast‐like differentiation of hDPCs. The abundance of micro RNA ‐135b (miR‐135b) was measured by quantitative real‐time reverse transcriptase polymerase chain reaction ( qRT ‐ PCR ) and in situ hybridization ( ISH ). Bioinformatic analyses combined with luciferase assays were utilized to identify the targets interacting with miR‐135b. Overexpression of miR‐135b was performed to investigate the role and mechanism in odontoblast‐like differentiation of hDPCs. Statistical analysis was performed by one‐way analysis of variance ( anova ) or Student's t ‐test. Results Thirty‐six differentially expressed micro RNA s in odontoblast‐like differentiation of hDPCs were identified. MiR‐135b expression was significantly downregulated during hDPCs differentiation ( P < 0.05). In addition, miR‐135b was able to bind to the 3′‐ UTR of the Smad5 and Smad4 and repressed these two genes expression ( P < 0.05). Furthermore, overexpression of miR‐135b suppressed odontoblast‐like differentiation of hDPCs and attenuated the expression of Smad5 and Smad4 ( P < 0.05). Conclusions These observations indicated a potential role of miR‐135b in mediating odontoblast‐like differentiation of hDPCs and inhibition of miR‐135b might be a promising therapeutic way to facilitate dentine tissue engineering.