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The miR‐3940‐5p inhibits cell proliferation of gingival mesenchymal stem cells
Author(s) -
Han Xiao,
Yang Haoqing,
Cao Yangyang,
Ge Lihua,
Han Nannan,
Zhang Chen,
Fan Zhipeng,
Yao Rui
Publication year - 2019
Publication title -
oral diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.953
H-Index - 87
eISSN - 1601-0825
pISSN - 1354-523X
DOI - 10.1111/odi.13092
Subject(s) - mesenchymal stem cell , cell growth , cell cycle , alkaline phosphatase , cyclin d1 , chemistry , stem cell , cellular differentiation , cell , microbiology and biotechnology , cancer research , biology , biochemistry , enzyme , gene
Objectives Drug‐induced gingival overgrowth (DIGO) is a well‐recognized side effect of nifedipine (NIF). However, the molecular mechanisms of DIGO are still unknown. Here, we explored the possible role of miR‐3940‐5p in DIGO using NIF‐treated gingival mesenchymal stem cells (GMSCs). Material and methods CFSE and cell cycle assays were used to examine cell proliferation. The alkaline phosphatase (ALP) activity assay, Alizarin Red staining, quantitative calcium analysis, and osteogenesis‐related gene expression were used to examine osteo/dentinogenic differentiation. Results The CFSE assay showed that NIF enhanced cell proliferation, and the over‐expression of miR‐3940‐5p inhibited the proliferation of GMSCs with or without NIF stimulation. Cell cycle assays revealed that the cell cycle was arrested at the G0/G1 phase. Furthermore, it was found that the over‐expression of miR‐3940‐5p upregulated p15 INK4b , p18 INK4c , p19 INK4d , and Cyclin A and downregulated Cyclin E in GMSCs with or without NIF treatment. In addition, the over‐expression of miR‐3940‐5p enhanced ALP activity and mineralization in vitro and increased the expression of the osteo/dentinogenic differentiation markers DSPP and DMP1 and the key transcription factor DLX5 in GMSCs. Conclusions miR‐3940‐5p inhibited cell proliferation, enhanced the osteo/dentinogenic differentiation of GMSCs, and might play a role in DIGO as a potent agent in the treatment of nifedipine‐induced gingival overgrowth.