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- Author: Hyunsoo Kim x
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Asan Institute for Life Sciences, Seoul, Republic of Korea
Department of Cell and Developmental Biology, Dental Research Institute, Seoul National University, Seoul, Republic of Korea
Department of Thoracic and Cardiovascular Surgery, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Republic of Korea
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Asan Institute for Life Sciences, Seoul, Republic of Korea
Department of Cell and Developmental Biology, Dental Research Institute, Seoul National University, Seoul, Republic of Korea
Department of Thoracic and Cardiovascular Surgery, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Republic of Korea
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Asan Institute for Life Sciences, Seoul, Republic of Korea
Department of Cell and Developmental Biology, Dental Research Institute, Seoul National University, Seoul, Republic of Korea
Department of Thoracic and Cardiovascular Surgery, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Republic of Korea
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Asan Institute for Life Sciences, Seoul, Republic of Korea
Department of Cell and Developmental Biology, Dental Research Institute, Seoul National University, Seoul, Republic of Korea
Department of Thoracic and Cardiovascular Surgery, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Republic of Korea
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Asan Institute for Life Sciences, Seoul, Republic of Korea
Department of Cell and Developmental Biology, Dental Research Institute, Seoul National University, Seoul, Republic of Korea
Department of Thoracic and Cardiovascular Surgery, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Republic of Korea
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Asan Institute for Life Sciences, Seoul, Republic of Korea
Department of Cell and Developmental Biology, Dental Research Institute, Seoul National University, Seoul, Republic of Korea
Department of Thoracic and Cardiovascular Surgery, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Republic of Korea
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Asan Institute for Life Sciences, Seoul, Republic of Korea
Department of Cell and Developmental Biology, Dental Research Institute, Seoul National University, Seoul, Republic of Korea
Department of Thoracic and Cardiovascular Surgery, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Republic of Korea
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Asan Institute for Life Sciences, Seoul, Republic of Korea
Department of Cell and Developmental Biology, Dental Research Institute, Seoul National University, Seoul, Republic of Korea
Department of Thoracic and Cardiovascular Surgery, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Republic of Korea
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Growing evidence has shown a biochemical link between increased oxidative stress and reduced bone density. Although α-lipoic acid (α-LA) has been shown to act as a thiol antioxidant, its effect on bone cells has not been determined. Using proteomic analysis, we identified six differentially expressed proteins in the conditioned media of α-LA-treated human bone marrow stromal cell line (HS-5). One of these proteins, receptor activator of nuclear factor κB ligand (RANKL), was significantly up-regulated, as confirmed by immunoblotting with anti-RANKL antibody. ELISA showed that α-LA stimulated RANKL production in cellular extracts (membranous RANKL) about 5-fold and in conditioned medium (soluble RANKL) about 23-fold, but had no effect on osteoprotegerin (OPG) secretion. Despite increasing the RANKL/OPG ratio, α-LA showed a dose-dependent suppression of osteoclastogenesis, both in a coculture system of mouse bone marrow cells and osteoblasts and in a mouse bone marrow cell culture system, and reduced bone resorption in a dose-dependent manner. In addition, α-LA-induced soluble RANKL was not inhibited by matrix metalloprotease inhibitors, indicating that soluble RANKL is produced by α-LA without any posttranslational processing. In contrast, α-LA had no significant effect on the proliferation and differentiation of HS-5 cells. These results suggest that α-LA suppresses osteoclastogenesis by directly inhibiting RANKL–RANK mediated signals, not by mediating cellular RANKL production. In addition, our findings indicate that α-LA-induced soluble RANKL is not produced by shedding of membranous RANKL.
