Bone formation is actively balanced via interaction between osteoblast
and osteoclast (17).
Our recent work has provided fundamental insights into the organization of the bone vasculature in mouse, its changes during aging, the heterogeneity and functional specialization of bone capillaries and endothelial cells, the regulation of these properties by notch and hypoxia-inducible factor signaling, and the crosstalk with osteoblast
MC3T3-E1 cells are a clonal preosteoblastic cell line derived from newborn mouse calvarias, which is utilized in many osteoblast
Interleukin 6 and Interleukin 17a enhance proliferation and differentiation of murine osteoblast
and human foetal osteoblast
In addition, we proved that primary prostate cancer lesions of BM+ patients were characterized by the expression of osteogenic molecules able to induce osteoblast
differentiation and to increase osteoblast
function such as mineralization.
Antidifferentiation ncRNA (ANCR) inhibits Runx2 expression in association with the enhancer of zeste homolog 2 (EZH2); thus, downregulation of ANCR promotes osteoblast
differentiation through modulation of EZH2/Runx2 .
They are able to give rise to osteoblast
cells and express factors and cytokines that support HSCs.
However, few studies had reported the direct evidence on the effect of [gamma]-tocotrienol in osteoblast
Unfortunately to date, only few studies have investigated the role of some lncRNAs (ANCR, H19, MEG, DANCR, etc.) on bone metabolism and they principally focused on osteoblast
differentiation and function, without taking in consideration the role of these ncRNAs as biomarkers for osteoporosis [28-30].
In this study, hybrid technology of sandblast, acid etching, and hydrothermal (HT) were used to form the micronanopermeable surface ofTi, and the effects ofthese Ti material on osseointegration were achieved by using MC3T3-E1 osteoblast
cell line proliferation, adhesion, spreading, and differentiation model.
For example, TNF[alpha] inhibits bone formation via multiple mechanisms, including inhibition of osteoblast
differentiation and mineralization and suppression of type I collagen synthesis and alkaline phosphatase activity [14, 17-19].
hOST: Primary human osteoblasts
(hOST, Lonza, Switzerland) were cultured in osteoblast
growth medium (OGM, Lonza, Switzerland) which maintains the proliferative phenotype.