1α,25‐dihydroxyvitamin D3 inhibits cell growth and chondrogenesis of a clonal mouse EC cell line, ATDC5 (original) (raw)
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Department of Orthopaedic Surgery, Kyoto University Faculty of Medicine, Kyoto, Japan
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Department of Biochemistry, Osaka University Faculty of Dentistry, Osaka, Japan
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Calcium Laboratory, Department of Radiology & Nuclear Medicine, Kyoto University Faculty of Medicine, Kyoto, Japan
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Department of Orthopaedic Surgery, Kyoto University Faculty of Medicine, Kyoto, Japan
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Department of Biochemistry, Osaka University Faculty of Dentistry, Osaka, Japan
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Department of Orthopaedic Surgery, Kyoto University Faculty of Medicine, Kyoto, Japan
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,
Department of Orthopaedic Surgery, Kyoto University Faculty of Medicine, Kyoto, Japan
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,
Department of Biochemistry, Osaka University Faculty of Dentistry, Osaka, Japan
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,
Calcium Laboratory, Department of Radiology & Nuclear Medicine, Kyoto University Faculty of Medicine, Kyoto, Japan
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Department of Orthopaedic Surgery, Kyoto University Faculty of Medicine, Kyoto, Japan
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Published:
01 January 1996
Revision received:
03 December 2009
Cite
Haruhiko Akiyama, Yuji Hiraki, Chohei Shigeno, Hiroaki Kohno, Chisa Shukunami, Tadao Tsuboyama, Ryuichi Kasai, Fujio Suzuki, Junji Konishi, Takashi Nakamura, 1α,25‐dihydroxyvitamin D3 inhibits cell growth and chondrogenesis of a clonal mouse EC cell line, ATDC5, Journal of Bone and Mineral Research, Volume 11, Issue 1, 1 January 1996, Pages 22–28, https://doi.org/10.1002/jbmr.5650110105
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Abstract
Here we report the effects of lα,25‐dihydroxyvitamin D3 [1,25(OH)2D3] in vitro on the growth and chondrogenesis of a chondroprogenitor‐like clonal mouse EC cell line, 10−10 to 10−7 M ATDC5, 1,25(OH)2D3 inhibited [3H]thymidine incorporation in undifferentiated chondroprogenitor‐like ATDC5 cells in time‐ and dose‐dependent manners. 1,25(OH)2D3 suppressed cartilage‐nodule formation and the accumulation of cartilage‐specific proteoglycan in ATDC5 cells in a dose‐dependent manner. The 1,25(OH)2D3‐induced inhibition of cartilage‐nodule formation was reversible and direct, unrelated to the antiproliferative action of the hormone on the undifferentiated ATDC5 cells. ATDC5 cells even in the precartilaginous stage expressed 4.4 kb vitamin D receptor (VDR) mRNA as assessed by northern blot analysis. The equilibrium saturation binding experiment revealed the presence of a single class of saturable and high‐affinity binding sites for 1,25(OH)2D3 in the cytosols. These results provide evidence for the hypothesis that both recruitment and chondrogenesis of chondroprogenitors are negatively regulated by 1,25(OH)2D3 via a VDR‐mediated process in vivo.
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