bone resorption/hypoxia

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Hypoxia induces giant osteoclast formation and extensive bone resorption in the cat.

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Dental disease due to osteoclast (OC) overactivity reaches epidemic proportions in older domestic cats and has also been reported in wild cats. Feline odontoclastic resorptive lesions (FORL) involve extensive resorption of the tooth, leaving it liable to root fracture and subsequent loss. The

Bone resorption facilitates osteoblastic bone metastatic colonization by cooperation of insulin-like growth factor and hypoxia.

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Bone metastasis is a multistep process that includes cancer cell dissemination, colonization, and metastatic growth. Furthermore, this process involves complex, reciprocal interactions between cancer cells and the bone microenvironment. Bone resorption is known to be involved in both osteolytic and

Constant hypoxia inhibits osteoclast differentiation and bone resorption by regulating phosphorylation of JNK and IκBα.

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Osteoclasts are responsible for the bone loss in rheumatoid arthritis (RA). Hypoxia has been suggested to play key roles in pathological bone loss. However, the current understanding of the effects of hypoxia on osteoclastogenesis is controversial. Effects of hypoxia on both the

Hypoxia-inducible factor 1-alpha does not regulate osteoclastogenesis but enhances bone resorption activity via prolyl-4-hydroxylase 2.

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Osteogenic-angiogenic coupling is promoted by the hypoxia-inducible factor 1-alpha (HIF-1α) transcription factor, provoking interest in HIF activation as a therapeutic strategy to improve osteoblast mineralization and treat pathological osteolysis. However, HIF also enhances the bone-resorbing

Hypoxia-inducible factor regulates osteoclast-mediated bone resorption: role of angiopoietin-like 4.

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Hypoxia and the hypoxia-inducible factor (HIF) transcription factor regulate angiogenic-osteogenic coupling and osteoclast-mediated bone resorption. To determine how HIF might coordinate osteoclast and osteoblast function, we studied angiopoietin-like 4 (ANGPTL4), the top HIF target gene in an

Sirtuin 6 suppresses hypoxia-induced inflammatory response in human osteoblasts via inhibition of reactive oxygen species production and glycolysis-A therapeutic implication in inflammatory bone resorption.

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Elevated glycolytic activity and redox imbalance induced by tissue hypoxia are common phenomena of chronic inflammation, including inflammatory bone diseases such as arthritis. However, relation between glycolysis and redox signaling in the inflammatory milieu is unclear. The histone deacetylase

Hypoxia is a major stimulator of osteoclast formation and bone resorption.

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Hypoxia is known to act as a general stimulator of cells derived from marrow precursors. We investigated the effect of oxygen tension on the formation and function of osteoclasts, the cells responsible for bore resorption, which are of promonocytic origin. Using 7- and 13-day cultures of mouse

'Hypoxia-inducible factor 1-alpha does not regulate osteoclastogenesis but enhances bone resorption activity via prolyl-4-hydroxylase 2'.

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Bu-Shen-Tong-Luo decoction prevents bone loss via inhibition of bone resorption and enhancement of angiogenesis in ovariectomy-induced osteoporosis of rats.

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BACKGROUND Gathering three ancient formulas, traditional Chinese medicine Bu-Shen-Tong-Luo decoction (BSTLD) has been used to treat postmenopausal osteoporosis (PMO) at the Jiangsu Province Hospital of Chinese Medicine for decades. However, the effect of BSTLD on angiogenesis and bone resorption as

Long-term exposure to hypobaric hypoxia in rat affects femur cross-sectional geometry and bone tissue material properties.

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Hypoxia leads to an increase in erythropoiesis, which induces hypertrophy of the erythropoietic marrow and may induce bone resorption. This study investigates the effect of chronic hypobaric hypoxia (simulated high altitude, SHA) on the biomechanics of rat femurs by mechanical tests of diaphyseal

Hypoxia stimulates vesicular ATP release from rat osteoblasts.

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Many neuronal and non-neuronal cell types release ATP in a controlled manner. After release, extracellular ATP (or, following hydrolysis, ADP) acts on cells in a paracrine manner via P2 receptors. Extracellular nucleotides are now thought to play an important role in the regulation of bone cell

Separate and combined effects of hypobaric hypoxia and hindlimb suspension on skeletal homeostasis and hematopoiesis in mice.

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Bone marrow response to an organismal stress is made by orchestrating the interplay between hematopoietic stem/progenitor cells (HSPCs) and mesenchymal stromal cells (MSCs). Neither the cellular nor the molecular factors that regulate this process are fully understood, especially since

Effect of hypoxia on the expression of RANKL/OPG in human periodontal ligament cells in vitro.

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To investigate the impact of hypoxia on the expression of receptor activator of NF-kB ligand (RANKL) and osteoprotegerin (OPG) in human periodontal ligament cells (hPDLCs) in vitro. hPDLCs were incubated in a hypoxic atmosphere of 2% O2, 5% CO2, 94% N2 at 37°C for 6, 12, 24 and 48 h. After that,

Compression and hypoxia play independent roles while having combinative effects in the osteoclastogenesis induced by periodontal ligament cells.

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OBJECTIVE To investigate the isolated and combined effects of compression and hypoxia on the osteoclastogenesis induced by periodontal ligament cells (PDLCs). METHODS A periodontal ligament tissue model (PDLtm) was established by 3-D culturing human PDLCs on a thin sheet of poly lactic-co-glycolic

Hypoxia mediates osteocyte ORP150 expression and cell death in vitro.

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Skeletal unloading leads to hypoxia in the bone microenvironment, resulting in imbalanced bone remodeling that favors bone resorption. Osteocytes, the mechanosensors of bone, have been demonstrated to orchestrate bone homeostasis. Hypoxic osteocytes either undergo apoptosis or actively stimulate

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