XXXX Exposure Accelerates Endochondral Ossification of @entity1573 Embryos Via Angiogenesis.

@entity1 @entity57831 @entity9170 @entity19 @entity619 @entity1573 @entity57830
UNASSIGNED: @entity619 ( @entity9170 ) is widely used to treat chronic inflammatory diseases in the clinic. Increasingly, there is more attention being paid to the side effect of @entity9170 . In this study, we investigated the involvement and mechanism of @entity9170 exposure in accelerating mineralization during long bone formation. We first determined that @entity9170 exposure could accelerate long bone mineralization in  vivo, but there was no apparent difference between control and @entity9170 -treated in the phalanges model in  vitro. Next, we established that @entity9170 exposure promoted angiogenesis in the @entity1573 yolk sac membrane model. In addition, it increased @entity1 umbilical vein endothelial cell proliferation and migration in culture. We found that @entity9170 could enhance angiogenesis when phalanges were cultured on @entity1573 chorioallantoic membrane and correspondingly increased the expression of angiogenesis-related genes in the phalanges. Furthermore, we also revealed that @entity9170 exposure reduced the number of osteoblasts and simultaneously increased the number of osteocytes in ex vivo-cultured phalanges. @entity57830 and @entity57831 expressions were up-regulated by @entity9170 exposure, indicating that @entity9170 exposure accelerated the terminal differentiation of osteoblasts. Lastly, we demonstrated that @entity19 cells cultured in the presence of @entity9170 accelerated their mineralization. In summary, we have shown that the ability of @entity9170 to initiate angiogenesis is the mechanism that allows it to accelerate mineralization during long bone formation.
