Open AccessEffects of neurotrophin receptor‐mediated MAGE homology on proliferation and odontoblastic differentiation of mouse dental pulp cells
Author(s) -
Qi S.,
Wu Q.,
Ma J.,
Li J.,
Chen F.,
Xu Y.,
Pan Q.,
Wang R.
Publication year - 2015
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/cpr.12171
Subject(s) - gene knockdown , neurotrophin , chemistry , microbiology and biotechnology , messenger rna , cytoplasm , cell growth , pulp (tooth) , nucleus , receptor , biology , gene , pathology , medicine , biochemistry
Objectives This study aimed to investigate effects of neurotrophin receptor‐mediated melanoma antigen‐encoding gene homology ( NRAGE ) on proliferation and odontoblastic differentiation of mouse dental pulp cells ( mDPC s). Materials and methods Mouse dental pulp cells were infected with recombinant lentivirus to stably knockdown expression of NRAGE , and biological effects of NRAGE on the cells were detected. Proliferation and odontoblastic differentiation of mDPC s were observed. Simultaneously, mRNA and protein levels of NRAGE and nuclear factor‐κB (NF‐κB) protein expression were detected. Immunofluorescence assay was used to detect expression and location of NRAGE and NF ‐κB. Results NRAGE mRNA and protein levels reduced significantly after mDPC odontoblastic induction. Knockdown of NRAGE inhibited the proliferation of mDPC s. However, knockdown of NRAGE enhanced their odontoblastic differentiation with up‐regulated ALP ase activity. It also promoted mineral nodule formation as well as mRNA and protein expressions of ALP , DSPP and DMP 1. Protein levels of NF ‐κB/p50 significantly increased, whereas NF ‐κB/p105 protein expression decreased in the mDPC /sh NRG group. Immunofluorescence revealed that relocation of NF ‐κB was similar to that of NRAGE during odontoblastic induction, in which NF ‐κB translocated from the cytoplasm to the nucleus. Conclusion NRAGE is a potent regulator of proliferation and odontoblastic differentiation of mDPC s, which might be via the NF ‐κB signalling pathway.