Targeted ablation of osteocytes induces osteoporosis with defective mechanotransduction.
By S. Tatsumi, Kiyo-aki Ishii, N. Amizuka, Minqi Li, Toshihiro Kobayashi, K. Kohno, Masako Ito, S. Takeshita, K. Ikeda. Cell Metabolism, 2007
865 citations recorded by the source corpus.
Subfields: Cell Biology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/64f0538ec5d6d6da008d7fa9892d0a930d6776bd
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Citations in the corpus
- Osteocytes, mechanosensing and Wnt signaling. (2008, background): “These studies show that osteocytes are necessary to maintain bone mass in response to normal load, but in the absence of load send signals of resorption [113].”
- Receptor activator of nuclear factor kappaB ligand and osteoprotegerin regulation of bone remodeling in health and disease. (2008, neutral): “The conditional ablation of osteoctyes in mice was associated with rapid bone loss in association with increased bone resorption, increased skeletal expression of RANKL mRNA, and an increased RANKL:OPG ratio (123).”
- Sclerostin Mediates Bone Response to Mechanical Unloading Through Antagonizing Wnt/β‐Catenin Signaling (2009, background): “ical signaling), as targeted ablation of osteocyte diminishes bone response to unloading.((4)) A number of important molecules were shown in vitro and in vivo to be modulated in osteocytes in response to increased mechanical stress, including ATP, NO, prostaglandin E2 (PGE-2), IGF-1,”
- Disorders of bone remodeling. (2011, background): “The central role of osteocytes in adapting bone properties to mechanical loading was convincingly demonstrated by a recent study (132) showing that genetically modified mice lacking osteocytes develop osteoporosis due to defective mechanotransduction.”
- Matrix-embedded cells control osteoclast formation (2011, background): “A recent study using an inducible osteocyte ablation model showed that osteocyte apoptosis leads to bone resorption associated with increased RANKL expressio”
- The Amazing Osteocyte (2010, methodology): “Targeted ablation of osteocytes through necrosis was performed using the 10-kb Dmp1 promoter to drive the diptheria toxin receptor expression in osteocytes.((33)) Injection of a single dose of diphtheria toxin eliminated approximately 70% of osteocytes in cortical bone and generated osteoclast activ”