Exosomes derived from idiopathic gingival fibroma fibroblasts regulate gingival fibroblast proliferation and apoptosis

Objective Exosomes have been proved to play an essential role in intercellular information transmission. However, few researches focused on exosomes derived from gingival fibroblasts (GFs) of IGF. The aim of this study is to investigate the effect of exosomes derived from GFs of IGF (IGF‐GFs) on the...

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Veröffentlicht in:Oral diseases 2021-10, Vol.27 (7), p.1789-1795
Hauptverfasser: Yin, Shunhui, Jia, Fengmei, Ran, Liquan, Xie, Liangkun, Wu, Zhiyao, Zhan, Yeming, Zhang, Yan, Zhang, Mingzhu
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Sprache:eng
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Zusammenfassung:Objective Exosomes have been proved to play an essential role in intercellular information transmission. However, few researches focused on exosomes derived from gingival fibroblasts (GFs) of IGF. The aim of this study is to investigate the effect of exosomes derived from GFs of IGF (IGF‐GFs) on the proliferation and apoptosis of normal gingival fibroblasts (N‐GFs). Methods Gingival fibroblasts were cultured and identified using immunocytochemistry. Exosomes were isolated with exosomes extraction kit and characterized by transmission electron microscopy (TEM) and flow cytometry. PKH67 labeling was further used to trace the intracellular distribution of the exosomes. And MTS assay was used to test the effective concentration and time course of IGF‐GFs‐derived exosomes. Furthermore, the expression of PCNA, Ki67, Bcl‐2, and Bax in N‐GFs was analyzed by qRT‐PCR and Western blot. Results Exosomes were isolated from IGF‐GFs; the identification of exosomes and gingival fibroblasts was successfully finished. Moreover, we found that N‐GFs co‐cultured with exosomes showed a great increase in PCNA and Bcl‐2 levels, and a moderate increase in Ki67 levels. By contrast, the levels of Bax were significantly reduced. Conclusion These results suggest that exosomes derived from idiopathic gingival fibroma fibroblasts are involved in the regulation of gingival fibroblast proliferation and apoptosis.
ISSN:1354-523X
1601-0825
DOI:10.1111/odi.13707