MiR-455-3p activates Nrf2/ARE signaling via HDAC2 and protects osteoblasts from oxidative stress

氧化应激 细胞生物学 化学 氧化磷酸化 生物 生物化学
作者
Shijun Zhang,Wenliang Wu,Guangjun Jiao,Ci Li,Haichun Liu
出处
期刊:International Journal of Biological Macromolecules [Elsevier]
卷期号:107: 2094-2101 被引量:39
标识
DOI:10.1016/j.ijbiomac.2017.10.080
摘要

The important role of miR-455-3p in the pathogenesis of bone metabolism associated diseases is gradually emerging. This study aims to ascertain the involvement of miR-455-3p and its underlying mechanisms in osteoporosis.The osteoblast cell lines MC3T3-E1 was treated with ferric ammonium citrate (FAC) to mimic a pathological environment for osteoporosis. The cytotoxic effect of iron overload was assessed by proliferation, apoptosis and oxidative stress of osteoblasts using commercial kits. Molecular biological methods, including qRT-PCR analysis, cell transfection and luciferase reporter assays were used to explain the role of miR-455-3p and its potential mechanisms in osteoblast apoptosis.FAC dramatically inhibited the proliferation of osteoblast cells MC3T3-E1 but increased the apoptosis. We also observed that FAC significantly down-regulated miR-455-3p in MC3T3-E1 cells but enhanced HDAC2 protein level. Moreover, miR-455-3p overexpression eliminated the effects of iron overload on osteoblast cell proliferation, apoptosis and oxidative stress. In addition, miR-455-3p regulated osteoblast cell proliferation, apoptosis and oxidative stress through regulating HDAC2-Nrf2/ARE signaling pathway. MiR-455-3p overexpression alleviated the oxidative stress injury in osteoporosis mice.Our results demonstrated that miR-455-3p activated Nrf2/ARE signal pathway through suppressing Keap1 via negative regulating HDAC2 protein level, thereby suppressing oxidative stress and promoting osteoblasts growth.
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