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Platelet-Derived Growth Factor Regulates the Biological Behavior of Oral Mucosal Fibroblasts by Inducing Cell Autophagy and Its Mechanism.
Wang, Jie; Yang, Lina; You, Jialing; Wen, Dada; Yang, Bo; Jiang, Canhua.
Afiliación
  • Wang J; Department of Oral and Maxillofacial Surgery, Xiangya Hospital, Central South University, Changsha, 410078, People's Republic of China.
  • Yang L; Department of Immunology, Xiangya School of Medicine, Central South University, Changsha, 410078, People's Republic of China.
  • You J; Department of Immunology, Xiangya School of Medicine, Central South University, Changsha, 410078, People's Republic of China.
  • Wen D; Department of Immunology, Xiangya School of Medicine, Central South University, Changsha, 410078, People's Republic of China.
  • Yang B; Department of Immunology, Xiangya School of Medicine, Central South University, Changsha, 410078, People's Republic of China.
  • Jiang C; Department of Immunology, Xiangya School of Medicine, Central South University, Changsha, 410078, People's Republic of China.
J Inflamm Res ; 14: 3405-3417, 2021.
Article en En | MEDLINE | ID: mdl-34305405
OBJECTIVE: To explore the effect of platelet-derived growth factor (PDGF) on oral mucosal fibroblast autophagy and further elucidate the molecular mechanism by which PDGF-BB regulates the biological behavior of oral mucosal fibroblasts by inducing autophagy. METHODS: Primary oral mucosal fibroblasts were isolated and cultured by the tissue block and trypsin methods and identified by indirect immunofluorescence vimentin detection. We detected the autophagy marker Beclin-1 and fibrosis marker Col-I of the primary oral mucosal fibroblasts at different time points after stimulating the fibroblasts with different PDGF-BB concentrations by Western blotting and determined the best experimental concentration and stimulation time of PDGF-BB. Then, indirect immunofluorescence, Western blotting, and quantitative real-time polymerase chain reaction (PCR) were used to detect the effect of PDGF-BB on the expression of autophagy-related and fibrotic proteins before and after 3-methyladenine (3-MA) intervention. Additionally, the effect of 3-MA on the proliferation and migration of primary oral mucosal fibroblasts stimulated by PDGF-BB was detected by the MTT method and a scratch experiment. The effect of PDGF-BB on Beclin-1 and phosphatidylinositol-3 kinase class 3 (PI3KC3) interaction was detected by co-immunoprecipitation. RESULTS: The results demonstrated that PDGF-BB could induce autophagy of the oral mucosal fibroblasts, showing a certain time and dose correlation. It induced cell autophagy through Beclin-1 and PI3KC3 interaction to promote the proliferation, migration, conversion, and collagen synthesis of the fibroblasts. However, 3-MA inhibited the combination of Beclin-1 and PI3KC3 and weakened the fibroblasts' proliferation, migration, conversion, and collagen synthesis activities. CONCLUSION: Overall, PDGF-BB induces autophagy through the Beclin-1 pathway to regulate the biological behavior of oral mucosal fibroblasts.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Tipo de estudio: Prognostic_studies Idioma: En Revista: J Inflamm Res Año: 2021 Tipo del documento: Article Pais de publicación: Nueva Zelanda

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Tipo de estudio: Prognostic_studies Idioma: En Revista: J Inflamm Res Año: 2021 Tipo del documento: Article Pais de publicación: Nueva Zelanda