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Enhancer of zeste homolog 2 enhances the migration and chemotaxis of dental mesenchymal stem cells

OBJECTIVE: To investigate the function of enhancer of zeste homolog 2 (EZH2) in the migration and chemotaxis of human dental tissue-derived mesenchymal stem cells. METHODS: The expression of EZH2, C-X-C motif chemokine ligand 11 (CXCL11), CXCL16, and CXCR1 in stem cells from the apical papilla (SCAP...

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Detalles Bibliográficos
Autores principales: Ma, Huarui, Duan, Shaoyu, Yan, Fei, Yang, Haoqing, Cao, Yangyang, Ge, Lihua, Gao, Runtao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7262854/
https://www.ncbi.nlm.nih.gov/pubmed/31642363
http://dx.doi.org/10.1177/0300060519882149
Descripción
Sumario:OBJECTIVE: To investigate the function of enhancer of zeste homolog 2 (EZH2) in the migration and chemotaxis of human dental tissue-derived mesenchymal stem cells. METHODS: The expression of EZH2, C-X-C motif chemokine ligand 11 (CXCL11), CXCL16, and CXCR1 in stem cells from the apical papilla (SCAPs) was determined by real-time reverse transcription PCR and western blotting. The effects of EZH2 on the homing of SCAPs and the effects of EZH2-overexpressing SCAP culture supernatant on periodontal ligament stem cells (PDLSCs) were tested by scratch migration assays and transwell chemotaxis assays. RESULTS: EZH2 overexpression significantly enhanced the migration and chemotaxis of SCAPs and upregulated the expression of CXCL11, CXCL16, and CXCR1 in SCAPs. EZH2 depletion had the opposite effect, impairing the migration and chemotaxis of SCAPs and downregulating the expression of CXCL11, CXCL16, and CXCR1. The culture supernatant of EZH2-overexpressing SCAPs advanced the migration and chemotaxis of PDLSCs. CONCLUSIONS: EZH2 evidently promoted the migration and chemotaxis of SCAPs by upregulating the expression of CXCL11, CXCL16, and CXCR1. Moreover, EZH2-overexpressing SCAPs enhanced the homing, migration, and chemotaxis of PDLSCs via paracrine signaling.