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Silent Mating Type Information Regulation 2 Homolog (SIRT1) Influences Osteogenic Proliferation and Differentiation of MC3T3-E1 Cells via Regulation of miR-132-3p

BACKGROUND: The essence of osteoporosis is mainly the imbalance of bone formation and absorption. Previous studies indicated that SIRT1 is closely related to bone metabolism and bone mass as a regulator of bone mass. The literature reports that microRNAs are significant regulators of osteoblast prol...

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Detalles Bibliográficos
Autores principales: Qu, Hangbo, Li, Taoye, Jin, Hongting, Zhang, Shanxing, He, Bangjian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scientific Literature, Inc. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6451357/
https://www.ncbi.nlm.nih.gov/pubmed/30923307
http://dx.doi.org/10.12659/MSM.912392
Descripción
Sumario:BACKGROUND: The essence of osteoporosis is mainly the imbalance of bone formation and absorption. Previous studies indicated that SIRT1 is closely related to bone metabolism and bone mass as a regulator of bone mass. The literature reports that microRNAs are significant regulators of osteoblast proliferation and differentiation. MATERIAL/METHODS: In this study, SIRT1 protein and mRNA levels were examined by Western blot and RT-PCR. Osteogenic proliferation was examined by CCK8 assay and osteogenic markers, including ALP, OCN, and RUNX2, were examined by ELISA. The target of miR-132-3p was identified by luciferase reporter assay. RESULTS: LPS downregulated the SIRT1 protein level and β-glycerophosphate upregulated the SIRT1 protein level. The results demonstrated that SIRT1 overexpression promoted the proliferation and differentiation in MC3T3-E1 cells, and SIRT1 interference had the opposite effect. Luciferase reporter assay revealed that miR-132-3p inhibited the reporter gene activity of SIRT1. LPS upregulated the mRNA level of miR-132-3p, and β-glycerophosphate downregulated the mRNA level of miR-132-3p. CONCLUSIONS: miR-132-3p is a pivotal regulator in osteogenic proliferation and differentiation by targeting SIRT1.