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PGF and VEGF‐C secreted by preosteoclasts induce migration and differentiation of Mesenchymal stem cells
Author(s) -
Huh JeongEun,
Yi Sol,
Lee Soo Young
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.lb134
Subject(s) - osteoclast , osteoblast , vascular endothelial growth factor , mesenchymal stem cell , rankl , bone resorption , microbiology and biotechnology , chemistry , bone morphogenetic protein 2 , kinase insert domain receptor , rank ligand , growth factor , biology , vascular endothelial growth factor a , receptor , activator (genetics) , endocrinology , cancer research , biochemistry , in vitro , vegf receptors
Osteoblast‐mediated bone formation is coupled to osteoclast‐mediated bone resorption. Several studies suggested that the molecular mechanisms by which osteoblasts control osteoclastogenesis and bone degradation. But, the recruitment of mesenchymal stem cells (MSCs) and their differentiation to osteoblasts is poorly understood. Here we show that preosteoclasts secrete placental growth factor (PGF) and vascular endothelial growth factor C (VEGF‐C) to induce migration and osteogenesis of MSCs. Conditioned media from preosteoclasts increased migration ability of MSCs and alkaline phosphatase activity and mineralization in osteoblast cultures. Osteoclast precursors induced PGF and VEGF‐C expression in response to receptor activator of nuclear factor‐κB ligand (RANKL), an essential cytokine for osteoclast differentiation. In vitro experiments revealed that migration was stimulated by rhPGF and rhVEGF‐C in a dose‐dependent manner. Furthermore, these factors increased osteoblast differentiation. Vascular endothelial growth factor receptor (VEGFR) inhibitor treatment reduced these responses. Taken together, PGF and VEGF‐C secreted by preosteoclasts may enhance the recruitment of MSCs and further induce osteogenesis. Support or Funding Information This work was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (NRF‐ 2015R1D1A4A01020104). This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .