enhance bone formation
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2022 ◽  
Vol 13 (1) ◽  
Author(s):  
Ziang Xie ◽  
Lei Hou ◽  
Shuying Shen ◽  
Yizheng Wu ◽  
Jian Wang ◽  
...  

AbstractMechanical force is critical for the development and remodeling of bone. Here we report that mechanical force regulates the production of the metabolite asymmetric dimethylarginine (ADMA) via regulating the hydrolytic enzyme dimethylarginine dimethylaminohydrolase 1 (Ddah1) expression in osteoblasts. The presence of -394 4 N del/ins polymorphism of Ddah1 and higher serum ADMA concentration are negatively associated with bone mineral density. Global or osteoblast-specific deletion of Ddah1 leads to increased ADMA level but reduced bone formation. Further molecular study unveils that mechanical stimulation enhances TAZ/SMAD4-induced Ddah1 transcription. Deletion of Ddah1 in osteoblast-lineage cells fails to respond to mechanical stimulus-associated bone formation. Taken together, the study reveals mechanical force is capable of down-regulating ADMA to enhance bone formation.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jun Sun ◽  
Dong Yeon Shin ◽  
Mark Eiseman ◽  
Alisha R. Yallowitz ◽  
Na Li ◽  
...  

AbstractHedgehog signaling is essential for bone formation, including functioning as a means for the growth plate to drive skeletal mineralization. However, the mechanisms regulating hedgehog signaling specifically in bone-forming osteoblasts are largely unknown. Here, we identified SLIT and NTRK-like protein-5(Slitrk5), a transmembrane protein with few identified functions, as a negative regulator of hedgehog signaling in osteoblasts. Slitrk5 is selectively expressed in osteoblasts and loss of Slitrk5 enhanced osteoblast differentiation in vitro and in vivo. Loss of SLITRK5 in vitro leads to increased hedgehog signaling and overexpression of SLITRK5 in osteoblasts inhibits the induction of targets downstream of hedgehog signaling. Mechanistically, SLITRK5 binds to hedgehog ligands via its extracellular domain and interacts with PTCH1 via its intracellular domain. SLITRK5 is present in the primary cilium, and loss of SLITRK5 enhances SMO ciliary enrichment upon SHH stimulation. Thus, SLITRK5 is a negative regulator of hedgehog signaling in osteoblasts that may be attractive as a therapeutic target to enhance bone formation.


2019 ◽  
Vol 5 (9) ◽  
pp. 4587-4600 ◽  
Author(s):  
Bipin Gaihre ◽  
Janitha M. Unagolla ◽  
Jiayong Liu ◽  
Nabil A. Ebraheim ◽  
Ambalangodage C. Jayasuriya

Drug Delivery ◽  
2019 ◽  
Vol 26 (1) ◽  
pp. 137-146 ◽  
Author(s):  
Xue Yang ◽  
Huthayfa N.S Almassri ◽  
Qiongyue Zhang ◽  
Yihui Ma ◽  
Dan Zhang ◽  
...  

2018 ◽  
Vol 24 (23-24) ◽  
pp. 1775-1783 ◽  
Author(s):  
Anita Sanghani ◽  
Liza Osagie-Clouard ◽  
Soureouseh Samizadeh ◽  
Melanie Jean Coathup ◽  
Priya Kalia ◽  
...  

Bone Research ◽  
2018 ◽  
Vol 6 (1) ◽  
Author(s):  
Andrea E. Morrell ◽  
Genevieve N. Brown ◽  
Samuel T. Robinson ◽  
Rachel L. Sattler ◽  
Andrew D. Baik ◽  
...  

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