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      N-acetyl cysteine inhibits H 2O 2-mediated reduction in the mineralization of MC3T3-E1 cells by down-regulating Nrf2/HO-1 pathway

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          Abstract

          There are controversial findings regarding the roles of nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway on bone metabolism under oxidative stress. We investigated how Nrf2/HO-1 pathway affects osteoblast differentiation of MC3T3-E1 cells in response to hydrogen peroxide (H 2O 2), N-acetyl cysteine (NAC), or both. Exposing the cells to H 2O 2 decreased the alkaline phosphatase activity, calcium accumulation, and expression of osteoblast markers, such as osteocalcin and runt-related transcription factor-2. In contrast, H 2O 2 treatment increased the expression of Nrf2 and HO-1 in the cells. Treatment with hemin, a chemical HO-1 inducer, mimicked the inhibitory effect of H 2O 2 on osteoblast differentiation by increasing the HO-1 expression and decreasing the osteogenic marker genes. Pretreatment with NAC restored all changes induced by H 2O 2 to near normal levels in the cells. Collectively, our findings suggest that H 2O 2-mediated activation of Nrf2/HO-1 pathway negatively regulates the osteoblast differentiation, which is inhibited by NAC. [BMB Reports 2015; 48(11): 636-641]

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          Oxidative stress modulates osteoblastic differentiation of vascular and bone cells.

          N. Mody, F Parhami, T A Sarafian … (2001)
          Oxidative stress may regulate cellular function in multiple pathological conditions, including atherosclerosis. One feature of the atherosclerotic plaque is calcium mineral deposition, which appears to result from the differentiation of vascular osteoblastic cells, calcifying vascular cells (CVC). To determine the role of oxidative stress in regulating the activity of CVC, we treated these cells with hydrogen peroxide (H(2)O(2)) or xanthine/xanthine oxidase (XXO) and assessed their effects on intracellular oxidative stress, differentiation, and mineralization. These agents increased intracellular oxidative stress as determined by 2,7 dichlorofluorescein fluorescence, and enhanced osteoblastic differentiation of vascular cells, based on alkaline phosphatase activity and mineralization. In contrast, H(2)O(2) and XXO resulted in inhibition of differentiation markers in bone osteoblastic cells, MC3T3-E1, and marrow stromal cells, M2-10B4, while increasing oxidative stress. In addition, minimally oxidized low-density lipoprotein (MM-LDL), previously shown to enhance vascular cell and inhibit bone cell differentiation, also increased intracellular oxidative stress in the three cell types. These effects of XXO and MM-LDL were counteracted by the antioxidants Trolox and pyrrolidinedithiocarbamate. These results suggest that oxidative stress modulates differentiation of vascular and bone cells oppositely, which may explain the parallel buildup and loss of calcification, seen in vascular calcification and osteoporosis, respectively.
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            Effects of reactive oxygen species (ROS) on antioxidant system and osteoblastic differentiation in MC3T3-E1 cells.

            Yoshimitsu Abiko, Yorimasa Ogata, Yasuko Shibata … (2006)
            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.
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              Oxidative stress, free radicals and bone remodeling.

              Massimiliano Corsi Romanelli, Giuseppe Banfi, E Iorio (2007)
              Reactive oxygen species (ROS) are widely considered to be a causal factor in aging and in a number of pathological conditions, such as atherosclerosis, carcinogenesis and infarction. Their role in bone metabolism is dual, considering their effects under physiological or pathological conditions. Under physiological conditions, the production of ROS by osteoclasts helps accelerate destruction of calcified tissue, thus assisting in bone remodeling. In pathological conditions, when a bone fractures, e.g., radical generation is remarkably high. However, though the increases in osteoclastic activity and ROS production are linked in many skeletal pathologies, it remains to be clarified whether increased ROS production overwhelms antioxidant defenses, leaving the individual open to hyperoxidant stress.
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                Author and article information

                Journal
                Journal ID (nlm-ta): BMB Rep
                Journal ID (iso-abbrev): BMB Rep
                Journal ID (publisher-id): ksbmb
                Title: BMB Reports
                Publisher: Korean Society for Biochemistry and Molecular Biology
                ISSN (Print): 1976-6696
                ISSN (Electronic): 1976-670X
                Publication date (Print): November 2015
                Volume: 48
                Issue: 11
                Pages: 636-641
                Affiliations
                [1 ]Institute of Oral Biosciences and School of Dentistry
                [2 ]Department of Bioactive Material Sciences and Institute of Molecular Biology and Genetics, Chonbuk National University, Jeonju 54896
                [3 ]Department of Nursing, Chonnam Techno College, Chonnam 57500
                [4 ]Grassland and Forage Division, National Institute of Animal Science, RDA, Cheonan 31002, Korea
                Author notes
                [* ]Kyung-Yeol Lee, Tel: +82-63-270-4023; Fax: +82-63-270-4004; E-mail: kyleecnu@ 123456jbnu.ac.kr , Jeong-Chae Lee, Tel: +82-63-270-4049; Fax: +82-63-270-4004; E-mail: leejc88@ 123456jbnu.ac.kr
                [#]

                These authors contributed equally to this work.

                Article
                Publisher ID: BMB-48-636
                DOI: 10.5483/BMBRep.2015.48.11.112
                PMC ID: 4911206
                PubMed ID: 26303969
                SO-VID: 8259002e-bc62-4f31-b8c0-a0d4a0465a18
                Copyright © Copyright © 2015, Korean Society for Biochemistry and Molecular Biology
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 11 June 2015
                Date revision received : 06 July 2015
                Date accepted : 20 August 2015
                Categories
                Subject: Research-Article

                Keywords: h2o2,n-acetyl cysteine,nrf2,osteoblast differentiation,oxidative stress
                Data availability:
                Keywords: h2o2, n-acetyl cysteine, nrf2, osteoblast differentiation, oxidative stress

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