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Effects of reactive oxygen species (ROS) on antioxidant system and osteoblastic differentiation in MC3T3‐E1 cells
Author(s) -
Arai Masato,
Shibata Yasuko,
Pugdee Kamolparn,
Abiko Yoshimitsu,
Ogata Yorimasa
Publication year - 2007
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1080/15216540601156188
Subject(s) - oxidative stress , osteoblast , runx2 , reactive oxygen species , antioxidant , osteocalcin , chemistry , gene expression , microbiology and biotechnology , mineralization (soil science) , transcription factor , alkaline phosphatase , gene , biology , biochemistry , in vitro , enzyme , organic chemistry , nitrogen
Oxidative stress regulates cellular functions in multiple pathological conditions, including bone formation by osteoblastic cells. However, little is known about the cellular mechanisms responsible for the effects of oxidative stress on osteoblast functions in senescence. To clarify the inhibitory effects of oxidative stress on osteoblastic mineralization, we examined the relationship between the antioxidant system and bone formation in MC3T3‐E1 cells. After a single exposure to H2O2 within range of a non‐toxic concentration for cells, the mineralization level was diminished half. Under the same conditions, gene expression of the transcription factor Nrf2, which regulates antioxidant enzymes, was up‐regulated. In addition, gene expression for the osteogenic markers Runx2, ALP, and BSP was lower than that in non‐treated cells, whereas expression of the osteocalcin gene was up‐regulated following H2O2 exposure. These results suggest that reduced mineralization by MC3T3‐E1 cells after H2O2 exposure is the result of an up‐regulated antioxidant system and altered osteogenic gene expression.IUBMB Life, 59: 27‐33, 2007