Mechanism of action of estrogen on intramembranous bone formation: regulation of osteoblast differentiation and activity

Endocrinology ◽  
1992 ◽  
Vol 131 (2) ◽  
pp. 883-889 ◽  
Author(s):  
R. T. Turner
Keyword(s):  
Bone Formation ◽  
Mechanism Of Action ◽  
Osteoblast Differentiation ◽  
Intramembranous Bone ◽  
Intramembranous Bone Formation

scholarly journals Recent Advances of Osterix Transcription Factor in Osteoblast Differentiation and Bone Formation

2020 ◽  
Vol 8 ◽  
Author(s):  
Qian Liu ◽  
Mao Li ◽  
Shiyi Wang ◽  
Zhousheng Xiao ◽  
Yuanyuan Xiong ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Bone Formation ◽  
Osteoblast Differentiation ◽  
Bone Mineralization ◽  
Skeletal Development ◽  
Intramembranous Bone ◽  
Cartilage Differentiation ◽  
New Research ◽  
Intramembranous Bone Formation

With increasing life expectations, more and more patients suffer from fractures either induced by intensive sports or other bone-related diseases. The balance between osteoblast-mediated bone formation and osteoclast-mediated bone resorption is the basis for maintaining bone health. Osterix (Osx) has long been known to be an essential transcription factor for the osteoblast differentiation and bone mineralization. Emerging evidence suggests that Osx not only plays an important role in intramembranous bone formation, but also affects endochondral ossification by participating in the terminal cartilage differentiation. Given its essentiality in skeletal development and bone formation, Osx has become a new research hotspot in recent years. In this review, we focus on the progress of Osx’s function and its regulation in osteoblast differentiation and bone mass. And the potential role of Osx in developing new therapeutic strategies for osteolytic diseases was discussed.

Altered cartilage phenotype expressed during intramembranous bone formation

2009 ◽  
Vol 8 (11) ◽  
pp. 1377-1387 ◽  
Author(s):  
Kang Ting ◽  
Lee Ann Petropulos ◽  
Masaru Iwatsuki ◽  
Ichiro Nishimura
Keyword(s):  
Bone Formation ◽  
Intramembranous Bone ◽  
Intramembranous Bone Formation

scholarly journals Functional requirement of CCN2 for intramembranous bone formation in embryonic mice

2008 ◽  
Vol 366 (2) ◽  
pp. 450-456 ◽  
Author(s):  
Harumi Kawaki ◽  
Satoshi Kubota ◽  
Akiko Suzuki ◽  
Tomohiro Yamada ◽  
Tatsushi Matsumura ◽  
...  
Keyword(s):  
Bone Formation ◽  
Functional Requirement ◽  
Intramembranous Bone ◽  
Intramembranous Bone Formation

scholarly journals Transforming growth factor-beta and the initiation of chondrogenesis and osteogenesis in the rat femur.

1990 ◽  
Vol 110 (6) ◽  
pp. 2195-2207 ◽  
Author(s):  
M E Joyce ◽  
A B Roberts ◽  
M B Sporn ◽  
M E Bolander
Keyword(s):  
Growth Factor ◽  
Bone Formation ◽  
Fracture Healing ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Tgf Beta ◽  
Intramembranous Bone ◽  
Growth Factor Beta ◽  
Beta 2 ◽  
Intramembranous Bone Formation

We have investigated the ability of exogenous transforming growth factor-beta (TGF-beta) to induce osteogenesis and chondrogenesis, critical events in both bone formation and fracture healing. Daily injections of TGF-beta 1 or 2 into the subperiosteal region of newborn rat femurs resulted in localized intramembranous bone formation and chondrogenesis. After cessation of the injections, endochondral ossification occurred, resulting in replacement of cartilage with bone. Gene expression of type II collagen and immunolocalization of types I and II collagen were detected within the TGF-beta-induced cartilage and bone. Moreover, injection of TGF-beta 2 stimulated synthesis of TGF-beta 1 in chondrocytes and osteoblasts within the newly induced bone and cartilage, suggesting positive autoregulation of TGF-beta. TGF-beta 2 was more active in vivo than TGF-beta 1, stimulating formation of a mass that was on the average 375% larger at a comparable dose (p less than 0.001). With either TGF-beta isoform, the dose of the growth factor determined which type of tissue formed, so that the ratio of cartilage formation to intramembranous bone formation decreased as the dose was lowered. For TGF-beta 1, reducing the daily dose from 200 to 20 ng decreased the cartilage/intramembranous bone formation ratio from 3.57 to zero (p less than 0.001). With TGF-beta 2, the same dose change decreased the ratio from 3.71 to 0.28 (p less than 0.001). These data demonstrate that mesenchymal precursor cells in the periosteum are stimulated by TGF-beta to proliferate and differentiate, as occurs in embryologic bone formation and early fracture healing.

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