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Dikkopf-1 promotes matrix mineralization of osteoblasts by regulating Ca+-CAMK2A- CREB
Hyosun Park 1,2 (Graduate student), Sungsin Jo 1 (Research worker), Mi-Ae Jang3 (Professor), Sung Hoon Choi4 (Professor), Tae-Hwan Kim 1,2,5,* (Professor)
1Hanyang University Institute for Rheumatology Research,
2Translational Medicine, Graduate School of Biomedical Science and Engineering, Hanyang University,
3Laboratory Medicine and Genetics, Soonchunhyang University Bucheon Hospital, Soonchunhyang University College of Medicine,
4Orthopedic Surgery, Hanyang University Seoul Hospital,
5Rheumatology, Hanyang University Hospital for Rheumatic Diseases
Dickkopf-1 (DKK1) is a secreted protein that acts as an antagonist of the canonical WNT/モ-catenin pathway, which regulates osteoblast differentiation. However, the role of DKK1 on osteoblast differentiation has not yet been fully clarified. Here, we investigate the functional role of DKK1 on osteoblast differentiation. Primary osteoprogenitor cells were isolated from human spinal bone tissues. To examine the role of DKK1 in osteoblast differentiation, we manipulated the expression of DKK1, and the cells were differentiated into mature osteoblasts. DKK1 overexpression in osteoprogenitor cells promoted matrix mineralization of osteoblast differentiation but did not promote matrix maturation. DKK1 increased Ca+ influx and activation of the Ca+/calmodulin-dependent protein kinase II Alpha (CAMK2A)-cAMP response element-binding protein (CREB) and increased translocation of p-CREB into the nucleus. In contrast, stable DKK1 knockdown in human osteosarcoma cell line SaOS2 exhibited reduced nuclear translocation of p-CREB and matrix mineralization. Overall, we suggest that manipulating DKK1 regulates the matrix mineralization of osteoblasts by Ca+-CAMK2A-CREB, and DKK1 is a crucial gene for bone mineralization of osteoblasts.
Abstract, Accepted Manuscript(in press) [Submitted on June 23, 2022, Accepted on October 7, 2022]
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