S Qi1, Q Wu, J Ma, J Li, F Chen, Y Xu, Q Pan, R Wang. 1. Department of Stomatology, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, China.
Abstract
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 (mDPCs). 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 mDPCs 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 mDPCs. However, knockdown of NRAGE enhanced their odontoblastic differentiation with up-regulated ALPase activity. It also promoted mineral nodule formation as well as mRNA and protein expressions of ALP, DSPP and DMP1. Protein levels of NF-κB/p50 significantly increased, whereas NF-κB/p105 protein expression decreased in the mDPC/shNRG 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 mDPCs, which might be via the NF-κB signalling pathway.
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 (mDPCs). 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 mDPCs 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 mDPCs. However, knockdown of NRAGE enhanced their odontoblastic differentiation with up-regulated ALPase activity. It also promoted mineral nodule formation as well as mRNA and protein expressions of ALP, DSPP and DMP1. Protein levels of NF-κB/p50 significantly increased, whereas NF-κB/p105 protein expression decreased in the mDPC/shNRG 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 mDPCs, which might be via the NF-κB signalling pathway.
Authors: H Shibuya; H Iwata; N Masuyama; Y Gotoh; K Yamaguchi; K Irie; K Matsumoto; E Nishida; N Ueno Journal: EMBO J Date: 1998-02-16 Impact factor: 11.598