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Upregulation of embryonic stem cell marker Nanog in human gingival fibroblasts stimulated with cyclosporine A: An in vitro study

BACKGROUND/PURPOSE: Gingival overgrowth is a common side effect of medication with the immunosuppressant cyclosporine A (CsA). This study proposed to verify whether Nanog, an embryonic stem cell marker, contributes to gingival overgrowth stimulated with CsA in human gingival fibroblasts (HGFs). MATE...

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Detalles Bibliográficos
Autores principales: Yu, Cheng-Chia, Su, Ni-Yu, Liu, Chia-Ming, Yang, Li-Chiu, Tsai, Chung-Hung, Chang, Yu-Chao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Association for Dental Sciences of the Republic of China 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6395295/
https://www.ncbi.nlm.nih.gov/pubmed/30895027
http://dx.doi.org/10.1016/j.jds.2016.11.002
Descripción
Sumario:BACKGROUND/PURPOSE: Gingival overgrowth is a common side effect of medication with the immunosuppressant cyclosporine A (CsA). This study proposed to verify whether Nanog, an embryonic stem cell marker, contributes to gingival overgrowth stimulated with CsA in human gingival fibroblasts (HGFs). MATERIALS AND METHODS: The effect of CsA on HGFs was used to elucidate whether Nanog expression could be induced by CsA using quantitative real-time reverse transcription-polymerase chain reaction and Western blotting. Cell growth in CsA-treated HGFs with Nanog lentivirus-mediated short hairpin RNA interference knockdown was evaluated by tetrazolium bromide reduction assay. RESULTS: CsA upregulated Nanog transcript in HGFs in a dose-dependent manner (P < 0.05). CsA was also shown to increase Nanog protein expression in HGFs in a dose-dependent manner (P < 0.05). In addition, downregulation of Nanog by lentiviral infection significantly inhibited CsA-stimulated cell growth in HGFs (P < 0.05). CONCLUSION: CsA upregulated Nanog expression and cell growth in HGFs, while silencing Nanog effectively reversed these phenomena. Nanog may act as a major switch in the pathogenesis of CsA-induced gingival overgrowth.