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Influence of Angptl1 on osteoclast formation and osteoblastic phenotype in mouse cells

Authors
  • Ishida, Masayoshi1
  • Kawao, Naoyuki1
  • Mizukami, Yuya1
  • Takafuji, Yoshimasa1
  • Kaji, Hiroshi1
  • 1 Kindai University Faculty of Medicine, 377-2 Ohnohigashi, Osakasayama, Osaka, 589-8511, Japan , Osaka (Japan)
Type
Published Article
Journal
BMC Musculoskeletal Disorders
Publisher
Springer (Biomed Central Ltd.)
Publication Date
Apr 28, 2021
Volume
22
Issue
1
Identifiers
DOI: 10.1186/s12891-021-04278-6
Source
Springer Nature
Keywords
License
Green

Abstract

BackgroundOsteoblasts and osteoclasts play important roles during the bone remodeling in the physiological and pathophysiological states. Although angiopoietin family Angiopoietin like proteins (Angptls), including Angptl1, have been reported to be involved in inflammation, lipid metabolism and angiogenesis, the roles of Angptl1 in bone have not been reported so far.MethodsWe examined the effects of Angptl1 on the osteoblast and osteoclast phenotypes using mouse cells.ResultsAngptl1 significantly inhibited the osteoclast formation and mRNA levels of tartrate-resistant acid phosphatase and cathepsin K enhanced by receptor activator of nuclear factor κB ligand in RAW 264.7 and mouse bone marrow cells. Moreover, Angptl1 overexpression significantly enhanced Osterix mRNA levels, alkaline phosphatase activity and mineralization induced by bone morphogenetic protein-2 in ST2 cells, although it did not affect the expression of osteogenic genes in MC3T3-E1 and mouse osteoblasts. On the other hand, Angptl1 overexpression significantly reduced the mRNA levels of peroxisome proliferator-activated receptor γ and adipocyte protein-2 as well as the lipid droplet formation induced by adipogenic medium in 3T3-L1 cells.ConclusionsThe present study first indicated that Angptl1 suppresses and enhances osteoclast formation and osteoblastic differentiation in mouse cells, respectively, although it inhibits adipogenic differentiation of 3T3-L1 cells. These data suggest the possibility that Angptl1 might be physiologically related to bone remodeling.

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