, and b-catenin are the vital transcription factors for osteoblast differentiation (6).
CCL3 binds to its receptor, chemokine cytokine receptor 1, to inhibit the differentiation, proliferation, and osteogenic potential of osteoblasts by impairing mineralization activation by downregulating the expression of osteocalcin (OCN), runt-related transcription factor 2 (Runx2), and osterix
This activates the expression of runt-related transcription factor 2 (Runx2) and osterix
, which are the key transcription factors that induce osteoblast differentiation.
A 2017 study in Scientific Reports detailed how melatonin regulates the activity of a protein, Osterix
, that is crucial to the formation and activity of bone-building cells called osteoblasts.
If the Wnt/[beta]-catenin pathway remains active, [beta]-catenin translocated to the nucleus activates the expression of TCF/LEF dependent genes specific for osteogenic differentiation such as Runx2, Dlx5, and Osterix
, and at the same time the adipogenic genes C/EBP[alpha] and PPAR[gamma] are repressed [94-100].
Following vibration, cells were tested for osteoblast-specific transcription factor Osterix
(Osx) to detect osteoblastic differentiation.
Kunkel et al., "The novel zinc finger-containing transcription factor osterix
is required for osteoblast differentiation and bone formation," Cell, vol.
Ahmed et al., "Osterix
marks distinct waves of primitive and definitive stromal progenitors during bone marrow development," Developmental Cell, vol.
Decreased FOX1 suppresses osteoblastogenesis by decreasing osterix
and type 1 collagen protein levels but does not affect levels of Runx2 and Bsp (bone sialoprotein) .
Its activation stabilizes [beta]-catenin, a transcription factor that stimulates the production of osteoblastic transcription factors such as Runt-related transcription factor 2 (Runx2) and osterix
. Wnt/[beta]-catenin pathway activators such as the Wnt ligands thus raise the number of mineralizing osteoblasts and increase the rate of bone formation [18, 19].
Studies have shown thatintegrin-mediated activation of ERK1/2 pathway is responsible for regulating osteoblast differentiation through modulating transcription factors in the nucleus, including Runx2 (runt-related protein 2) and OSX (osterix
), downstream of Runx2 [31,32].
Insulin-like growth factor 1 receptor (IGF1R) signaling regulates osterix
expression and cartilage matrix mineralization during endochondral ossification.