scholarly journals Human autologous culture expanded bone marrow mesenchymal cell transplantation for repair of cartilage defects in osteoarthritic knees

2002 ◽  
Vol 10 (3) ◽  
pp. 199-206 ◽  
Author(s):  
S. Wakitani ◽  
K. Imoto ◽  
T. Yamamoto ◽  
M. Saito ◽  
N. Murata ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Cell Transplantation ◽  
Mesenchymal Cell ◽  
Cartilage Defects ◽  
Bone Marrow Mesenchymal Cell

scholarly journals Parathyroid Hormone Directs Bone Marrow Mesenchymal Cell Fate

2017 ◽  
Vol 25 (3) ◽  
pp. 661-672 ◽  
Author(s):  
Yi Fan ◽  
Jun-ichi Hanai ◽  
Phuong T. Le ◽  
Ruiye Bi ◽  
David Maridas ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Parathyroid Hormone ◽  
Cell Fate ◽  
Mesenchymal Cell ◽  
Bone Marrow Mesenchymal Cell

scholarly journals Bone marrow adipogenic lineage precursors (MALPs) promote osteoclastogenesis in bone remodeling and pathologic bone loss

2020 ◽  
Author(s):  
Wei Yu ◽  
Leilei Zhong ◽  
Lutian Yao ◽  
Yulong Wei ◽  
Tao Gui ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Loss ◽  
Trabecular Bone ◽  
Bone Remodeling ◽  
Mesenchymal Cell ◽  
Cell Network ◽  
Ovariectomized Mice ◽  
Drastic Increase ◽  
Trabecular Bone Mass ◽  
Bone Marrow Mesenchymal Cell

AbstractBone is maintained by coupled activities of bone-forming osteoblasts/osteocytes and bone-resorbing osteoclasts and an alternation of this relationship can lead to pathologic bone loss such as in osteoporosis. It is well known that osteogenic cells support osteoclastogenesis via synthesizing RANKL. Interestingly, our recently identified bone marrow mesenchymal cell population—marrow adipogenic lineage precursors (MALPs) that form a multi-dimensional cell network in bone—was computationally demonstrated to be the most interactive with monocyte-macrophage lineage cells through highly and specifically expressing several osteoclast regulatory factors, including RANKL. Using an adipocyte-specific Adipoq-Cre to label MALPs, we demonstrated that mice with RANKL deficiency in MALPs have a drastic increase of trabecular bone mass in long bones and vertebrae starting from 1 month of age but that their cortical bone is normal. This phenotype was accompanied by diminished osteoclast number and attenuated bone formation at the trabecular bone surface. Reduced RANKL signaling in calvarial MALPs also abolished osteolytic lesions after lipopolysaccharide (LPS) injections. Furthermore, in ovariectomized mice, elevated bone resorption was partially attenuated by RANKL deficiency in MALPs. In summary, our studies identified MALPs as a critical player in controlling bone remodeling during normal bone metabolism and pathological bone loss in a RANKL-dependent fashion.

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