scholarly journals Parathyroid Hormone Remodels Bone Transitional Vessels and the Leptin Receptor‐Positive Pericyte Network in Mice

2019 ◽  
Vol 34 (8) ◽  
pp. 1487-1501 ◽  
Author(s):  
Robin Caire ◽  
Bernard Roche ◽  
Tiphanie Picot ◽  
Carmen‐Mariana Aanei ◽  
Zhiguo He ◽  
...  
2021 ◽  
Vol 118 (25) ◽  
pp. e2026176118
Author(s):  
Jingzhu Zhang ◽  
Adi Cohen ◽  
Bo Shen ◽  
Liming Du ◽  
Alpaslan Tasdogan ◽  
...  

We previously described a new osteogenic growth factor, osteolectin/Clec11a, which is required for the maintenance of skeletal bone mass during adulthood. Osteolectin binds to Integrin α11 (Itga11), promoting Wnt pathway activation and osteogenic differentiation by leptin receptor+ (LepR+) stromal cells in the bone marrow. Parathyroid hormone (PTH) and sclerostin inhibitor (SOSTi) are bone anabolic agents that are administered to patients with osteoporosis. Here we tested whether osteolectin mediates the effects of PTH or SOSTi on bone formation. We discovered that PTH promoted Osteolectin expression by bone marrow stromal cells within hours of administration and that PTH treatment increased serum osteolectin levels in mice and humans. Osteolectin deficiency in mice attenuated Wnt pathway activation by PTH in bone marrow stromal cells and reduced the osteogenic response to PTH in vitro and in vivo. In contrast, SOSTi did not affect serum osteolectin levels and osteolectin was not required for SOSTi-induced bone formation. Combined administration of osteolectin and PTH, but not osteolectin and SOSTi, additively increased bone volume. PTH thus promotes osteolectin expression and osteolectin mediates part of the effect of PTH on bone formation.


2020 ◽  
Vol 99 (11) ◽  
pp. 1279-1286 ◽  
Author(s):  
D. Zhang ◽  
S. Zhang ◽  
J. Wang ◽  
Q. Li ◽  
H. Xue ◽  
...  

Stem cells play a critical role in bone regeneration. Multiple populations of skeletal stem cells have been identified in long bone, while their identity and functions in alveolar bone remain unclear. Here, we identified a quiescent leptin receptor–expressing (LepR+) cell population that contributed to intramembranous bone formation. Interestingly, these LepR+ cells became activated in response to tooth extraction and generated the majority of the newly formed bone in extraction sockets. In addition, genetic ablation of LepR+ cells attenuated extraction socket healing. The parabiosis experiments revealed that the LepR+ cells in the healing sockets were derived from resident tissue rather than peripheral blood circulation. Further studies on the mechanism suggested that these LepR+ cells were responsive to parathyroid hormone/parathyroid hormone 1 receptor (PTH/PTH1R) signaling. Collectively, we demonstrate that LepR+ cells, a postnatal skeletal stem cell population, are essential for alveolar bone regeneration of extraction sockets.


2019 ◽  
Vol 34 (10) ◽  
pp. 1952-1963 ◽  
Author(s):  
Mengyu Yang ◽  
Atsushi Arai ◽  
Nobuyuki Udagawa ◽  
Lijuan Zhao ◽  
Daisuke Nishida ◽  
...  

1998 ◽  
Vol 5 (1) ◽  
pp. 137A-137A
Author(s):  
J MCCARTHY ◽  
D MISRA ◽  
A KANBOURSHAKIR ◽  
L MINICH ◽  
D LYKINS ◽  
...  

2019 ◽  
Vol 25 ◽  
pp. 56-57
Author(s):  
Robert Gaffey ◽  
Eric Pagan ◽  
Briette Karanfillian ◽  
Sahil Parikh ◽  
Ankit Shah
Keyword(s):  

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