Identification of miR-200c-3p as a major regulator of SaoS2 cells activation induced by fluoride

• Published in: Chemosphere (Oxford) 2018-05, Vol.199, p.694-701
• Main Authors: Jiang, Yuting, Yang, Yanmei, Wang, Hongge, Darko, Gottfried M., Sun, Dianjun, Gao, Yanhui
• Format: Article
• Language: English
• Subjects: BMP4/Smad pathway; MiR-200c-3p; Osteoblast activation; Proliferation; SaoS2; Skeletal fluorosis
• ISSN: 0045-6535; 1879-1298
• DOI: 10.1016/j.chemosphere.2018.01.095

The skeletal lesion of fluoride has become a major concern in many countries due to its damage to bone and joints and even leading to disability. Skeletal fluorosis is characterized by disturbance of bone metabolism, aberrant proliferation and activation of osteoblasts is critical for the pathogenesis. However, the mechanism underlying the osteotoxicity of fluoride has not been clearly illustrated and there is still limited information on the role of miRNAs in skeletal fluorosis. In this study, we found that NaF promoted SaoS2 proliferation and activation by activating BMP4/Smad pathway. NaF increased expression of miR-200c-3p and miR-200c-3p inhibitor reduced activation of SaoS2 induced by NaF via targeting Noggin to repress BMP4/Smad. These findings suggested an important regulatory role of miR-200c-3p on BMP4/Smad pathway during skeletal fluorosis. MiR-200c-3p might be a novel therapeutic target for skeletal fluorosis. •NaF promoted osteoblast activity of SaoS2 cells by activating BMP4/Smad pathway.•NaF upregulated miR-200c-3p that may be a therapeutic target for skeletal fluorosis.•BMP4/Smad activated by NaF was partly controlled by miR-200c-3p/Noggin.