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Sprouty2 inhibition promotes proliferation and migration of periodontal ligament cells
Author(s) -
Tanaka U,
Sanui T,
Fukuda T,
Toyoda K,
Taketomi T,
Atomura R,
Yamamichi K,
Maeda H,
Nishimura F
Publication year - 2015
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.12369
Subject(s) - periodontal fiber , microbiology and biotechnology , basic fibroblast growth factor , epidermal growth factor , cell growth , chemistry , growth factor , cell culture , biology , medicine , biochemistry , genetics , receptor , dentistry
Objectives We previously demonstrated that a dominant‐negative Sprouty2 (Spry2) mutation promotes osteoblast proliferation and differentiation after basic fibroblast growth factor ( bFGF ) and epidermal growth factor ( EGF ) stimulation, whereas it diminishes proliferation of gingival epithelial cells, thereby inducing favourable conditions for periodontal tissue regeneration. In this study, we investigated how Spry2 inhibition affects the cellular physiology of periodontal ligament ( PDL ) cells. Methods A total of 1‐17 PDL cells (multipotent clonal human PDL cell line) were stimulated with bFGF and EGF after transfection of Spry2 si RNA . Cell proliferation, migration, ALP staining, real‐time PCR , Western blot and immunofluorescence assays were performed. Results ERK 1/2 activation and proliferation of 1‐17 PDL cells were significantly upregulated by the addition of Spry2 si RNA in the presence of bFGF and EGF . In addition, Spry2 si RNA reduced transcription of osteogenesis‐related genes and ALP staining relative to control cells. Furthermore, it increased AKT /phosphatidylinositol 3‐kinase ( PI 3K) phosphorylation; consequently, Rac1 but not Cdc42 was activated, thereby promoting lamellipodia formation, cell proliferation and migration after stimulation by bFGF and EGF. Conclusion Spry2 combined with bFGF and EGF stimulation reduced PDL cell migration and proliferation with inducing osteoblastic differentiation. These in vitro findings may provide a molecular basis for novel therapeutic approaches for establishing periodontal tissue regeneration.