scholarly journals TGF‐β/Smad2 signalling regulates enchondral bone formation of Gli1 + periosteal cells during fracture healing

2020 ◽  
Vol 53 (11) ◽  
Author(s):  
Chenjie Xia ◽  
Qinwen Ge ◽  
Liang Fang ◽  
Huan Yu ◽  
Zhen Zou ◽  
...  
2015 ◽  
Vol 30 (9) ◽  
pp. 1572-1584 ◽  
Author(s):  
Tao Wang ◽  
Yongmei Wang ◽  
Alicia Menendez ◽  
Chak Fong ◽  
Muriel Babey ◽  
...  

Author(s):  
Elise F. Morgan ◽  
Jason Pittman ◽  
Anthony DeGiacomo ◽  
Daniel Cusher ◽  
Chantal M. J. de Bakker ◽  
...  

2020 ◽  
Author(s):  
Brya G Matthews ◽  
Francesca V Sbrana ◽  
Sanja Novak ◽  
Jessica L. Funnell ◽  
Ye Cao ◽  
...  

AbstractThe periosteum is the major source of cells involved in fracture healing. We sought to characterize differences in progenitor cell populations between periosteum and other bone compartments, and identify periosteal cells involved in fracture healing. The periosteum is highly enriched for progenitor cells, including Sca1+ cells, CFU-F and label-retaining cells. Lineage tracing with αSMACreER identifies periosteal cells that contribute to >80% of osteoblasts and ~40% of chondrocytes following fracture. A subset of αSMA+ cells are quiescent long-term injury-responsive progenitors. Ablation of αSMA+ cells impairs fracture callus formation. In addition, committed osteoblast-lineage cells contributed around 10% of osteoblasts, but no chondrocytes in fracture calluses. Most periosteal progenitors, particularly those that form osteoblasts, can be targeted by αSMACreER. We have demonstrated that the periosteum is highly enriched for skeletal stem and progenitor cells and there is heterogeneity in the populations of cells that contribute to mature lineages during periosteal fracture healing.


2011 ◽  
Vol 26 (11) ◽  
pp. 2597-2609 ◽  
Author(s):  
Rachel Grimes ◽  
Karl J Jepsen ◽  
Jennifer L Fitch ◽  
Thomas A Einhorn ◽  
Louis C Gerstenfeld

2018 ◽  
Vol 20 (1) ◽  
pp. 83 ◽  
Author(s):  
Gabriele Russow ◽  
Denise Jahn ◽  
Jessika Appelt ◽  
Sven Märdian ◽  
Serafeim Tsitsilonis ◽  
...  

Osteoporosis represents the most common bone disease worldwide and results in a significantly increased fracture risk. Extrinsic and intrinsic factors implicated in the development of osteoporosis are also associated with delayed fracture healing and impaired bone regeneration. Based on a steadily increasing life expectancy in modern societies, the global implications of osteoporosis and impaired bone healing are substantial. Research in the last decades has revealed several molecular pathways that stimulate bone formation and could be targeted to treat both osteoporosis and impaired fracture healing. The identification and development of therapeutic approaches modulating bone formation, rather than bone resorption, fulfils an essential clinical need, as treatment options for reversing bone loss and promoting bone regeneration are limited. This review focuses on currently available and future approaches that may have the potential to achieve these aims.


PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e81399 ◽  
Author(s):  
Alayna E. Loiselle ◽  
Shane A. J. Lloyd ◽  
Emmanuel M. Paul ◽  
Gregory S. Lewis ◽  
Henry J. Donahue

PLoS ONE ◽  
2011 ◽  
Vol 6 (9) ◽  
pp. e24847 ◽  
Author(s):  
Daisuke Sakai ◽  
Isao Kii ◽  
Kazuki Nakagawa ◽  
Hiroko N. Matsumoto ◽  
Masateru Takahashi ◽  
...  

Bone ◽  
2012 ◽  
Vol 50 (5) ◽  
pp. 1123-1129 ◽  
Author(s):  
Masaki Nagata ◽  
Hideyuki Hoshina ◽  
Minqi Li ◽  
Megumi Arasawa ◽  
Kohya Uematsu ◽  
...  

2020 ◽  
Author(s):  
Mari Akiyma

AbstractOsteoporosis and bone fracture decrease quality of life. Bone regeneration is a notable technique for osteoporosis treatment. A previous study reported that F-box and WD-40 domain-containing protein 2 (FBXW2) and osteocalcin have the same shape in the periosteum after 5 weeks. However, the osteoblastic functions of FBXW2 are not clear. In this study, double fluorescent immunostaining revealed a small amount of osteocalcin in the area of FBXW2 aggregation at 1 week, periosteal cells, and osteocalcin pushed toward the edge of periosteum, and, apart from FBXW2 tubes at 2 weeks, multilayered periosteum-derived cells at 3 weeks and sticking of osteocalcin in the periosteum with cells at 4 weeks. At 5 weeks, FBXW2 disappeared at the root of periosteum-derived cells, while osteocalcin and cells remained. Based on these results, it is hypothesized that FBXW2 maintains tissue shapes and prevents escape of inner periosteal cells, and the disappearance of FBXW2 causes migration of periosteum-derived cells out of the periosteum along with osteocalcin. Furthermore, FBXW2 may play a role in dynamic tissue remodeling and bone formation.


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