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ORIGINAL ARTICLE
Year : 2020  |  Volume : 63  |  Issue : 6  |  Page : 286-293

Glucocorticoid transiently upregulates mitochondrial biogenesis in the osteoblast


1 Department of Orthopedics, Taoyuan General Hospital, Ministry of Health and Welfare; Graduate School of Biotechnology and Bioengineering, Yuan Ze University, Taoyuan, Taiwan
2 Department of Surgery, Taoyuan General Hospital, Ministry of Health and Welfare, Taoyuan, Taiwan
3 Department of Orthopedics, Taoyuan General Hospital, Ministry of Health and Welfare, Taoyuan; Department of Biology and Anatomy, National Defense Medical Center, Taipei, Taiwan
4 Department of Animal Science, National Pingtung University of Science and Technology, Pingtung, Taiwan
5 Department of Animal Science and Technology; Institute of Biotechnology, National Taiwan University, Taipei, Taiwan
6 Graduate School of Biotechnology and Bioengineering; Department of Chemical Engineering and Materials Science, Yuan Ze University, Taoyuan, Taiwan

Correspondence Address:
Dr. Chao-Ling Yao
Department of Chemical Engineering and Materials Science, Yuan Ze University, Taoyuan
Taiwan
Dr. Shao-Yu Peng
Department of Animal Science, National Pingtung University of Science and Technology, Pingtung
Taiwan
Prof. Shinn-Chih Wu
Institute of Biotechnology, National Taiwan University, Taipei; Institute of Animal Science and Technology, National Taiwan University, Taipei
Taiwan
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Source of Support: None, Conflict of Interest: None


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DOI: 10.4103/CJP.CJP_51_20

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Glucocorticoid (GC)-induced bone loss is the most prevalent form of secondary osteoporosis. Previous studies demonstrated that long-term incubation of dexamethasone (DEX) induced oxidative stress and mitochondrial dysfunctions, consequently leading to apoptosis of differentiated osteoblasts. This DEX-induced cell death might be the main causes of bone loss. We previously described that DEX induced biphasic mitochondrial alternations. As GC affects mitochondrial physiology through several different possible routes, the short-term and long-term effects of GC treatment on mitochondria in the osteoblast have not been carefully characterized. Here, we examined the expression levels of genes that are associated with mitochondrial functions at several different time points after incubation with DEX. Mitochondrial biogenesis-mediated genes nuclear respiratory factor 1 (Nrf1) and Nrf2 were upregulated after 4-h incubation, and then declined after 24-h incubation, suggesting that mitochondrial biogenesis were transiently upregulated by DEX. In contrast, mitochondrial fusion gene optic atrophy 1 (Opa1) and mitofusin 2 (Mfn2) started to be elevated as the biogenesis started to decrease. Finally, the mitochondrial fission increased and apoptosis becomes prominent. Agree with the mitochondrial biphasic alterations hypothesis, the results suggested an early increase of mitochondrial activities and biogenesis upon DEX stimulation to the osteoblasts. The oxidative phosphorylation and inducible nitric oxide synthase levels increased results in oxidative stress accumulation, leading to mitochondrial fusion, and subsequently fission and triggering the apoptosis. Our results indicated that the primary effects of GC on mitochondria are promoting their functions and biogenesis. Mitochondrial breakdown and the activation of the apoptotic pathways appeared to be the secondary effect after long-term treatment.


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