Abstract
Coupling between osteoblast-mediated bone formation and osteoclast-mediated bone resorption maintains both mechanical integrity and mineral homeostasis. Zinc is required for the formation, mineralization, growth, and maintenance of bones. We examined the effects of zinc sulfate on osteoblastic differentiation of human periosteum-derived cells (hPDCs) and osteoclastic differentiation of THP-1 cells. Zinc sulfate enhanced the osteoblastic differentiation of hPDCs; however, it did not affect the osteoclastic differentiation of THP-1 cells. The levels of extracellular signaling-related kinase (ERK) were strongly increased during osteoblastic differentiation in zinc sulfate-treated hPDCs, compared with other mitogen-activated protein kinases (MAPKs). Zinc sulfate also promoted osteogenesis in hPDCs and THP-1 cells co-cultured with the ratio of one osteoclast to one osteoblast, as indicated by alkaline phosphatase levels, mineralization, and cellular calcium contents. In addition, the receptor activator of nuclear factor kappa B ligand (RANKL)/osteoprotegerin (OPG) ratio was decreased in the zinc sulfate-treated co-cultures. Our results suggest that zinc sulfate enhances osteogenesis directly by promoting osteoblastic differentiation and osteogenic activities in osteoblasts and indirectly by inhibiting osteoclastic bone resorption through a reduced RANKL/OPG ratio in co-cultured osteoblasts and osteoclasts.
Highlights
Bone remodeling is highly regulated to maintain a balance between osteoblast-mediated and osteoclast-mediated bone resorption
We previously examined that human periosteum-derived cells express mesenchymal stem cell (MSC) markers and have differentiation potential toward adipocytes, osteocytes, and chondrocytes [3,4,5,6]
We investigated the effects of zinc sulfate on three mitogen-activated protein kinases (MAPKs) signaling pathways (ERK, Jun N-terminal kinase (JNK), and p38 MAPK) during human periosteum-derived cells (hPDCs) osteoblastogenesis
Summary
Bone remodeling is highly regulated to maintain a balance between osteoblast-mediated and osteoclast-mediated bone resorption. An imbalance of those tightly coupled processes can cause diseases such as osteoporosis. We previously examined that human periosteum-derived cells (hPDCs) express MSC markers and have differentiation potential toward adipocytes, osteocytes, and chondrocytes [3,4,5,6]. We refer to hPDCs as human periosteum-derived MSCs. Treatment of MSCs with growth factors or trace minerals can promote osteogenic differentiation of MSCs, increasing the likelihood that MSCs can be used for bone tissue repair [3,4,7,8]
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