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osteoporosis/tyrosine
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Glucocorticoid-induced osteoporosis in the rat is prevented by the tyrosine phosphatase inhibitor, sodium orthovanadate.
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Glucocorticoid-induced osteoporosis is characterized by decreased osteoblast numbers and a marked impairment of new bone formation. We found that, in vitro, dexamethasone inhibits both preosteoblast proliferation and mitogenic kinase activity in response to mitogens, and that inhibition of protein
Proline-rich tyrosine kinase 2 regulates osteoprogenitor cells and bone formation, and offers an anabolic treatment approach for osteoporosis.
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Bone is accrued and maintained primarily through the coupled actions of bone-forming osteoblasts and bone-resorbing osteoclasts. Cumulative in vitro studies indicated that proline-rich tyrosine kinase 2 (PYK2) is a positive mediator of osteoclast function and activity. However, our investigation of
Opposing effects of tyrosine kinase inhibitors on mineralization of normal and tumor bone cells.
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Induction of matrix maturation and mineralization in calcified tissues is important for patients with primary bone tumors and other bone deficiencies, e.g., osteoporosis. For the former it signifies a better prognosis in osteosarcoma, and for the latter it might improve bone remodeling. In the
High-throughput metabolomics investigates anti-osteoporosis activity of oleanolic acid via regulating metabolic networks using ultra-performance liquid chromatography coupled with mass spectrometry.
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BACKGROUND
Osteoporosis has brought about heavy socio-economic burden in the morbidity and medical expenses associated with osteoporosis treatment and various restrictions on behavior of their social roles. Oleanolic acid (OA) is an anti-osteoporosis natural product, but molecular mechanisms of
Novel bone-targeted Src tyrosine kinase inhibitor drug discovery.
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Bone-targeted Src tyrosine kinase (STK) inhibitors have recently been developed for the treatment of osteoporosis and cancer-related bone diseases. The concept of bone targeting derives from bisphosphonates, and from the evolution of such molecules in terms of therapeutic efficacy for the treatment
The tyrosine kinase inhibitor GNF-2 suppresses osteoclast formation and activity.
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GNF-2, a tyrosine kinase inhibitor, was developed to overcome imatinib-resistant mutations found in CML patients. Osteoclasts are the principal bone-resorbing cells that are responsible for bone diseases, such as osteoporosis, tumor-induced osteolysis, and metastatic cancers. In this study, we
Tyrosine kinase inhibition in bone metabolism.
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Inhibition of tyrosine kinase signaling has become increasingly important as a therapeutic approach for a variety of diseases, initially for cancer, but also for inflammatory and non-malignant hyperproliferative diseases (psoriasis) amongst others. Recently, inhibitors of the tyrosine kinase c-Src,
Src inhibitors: drugs for the treatment of osteoporosis, cancer or both?
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Src was one of the first proto-oncogenes to be identified and is a prototype of non-receptor type tyrosine kinases. The role of Src in bone metabolism first became apparent in Src-deficient mice and has been confirmed using low-molecular-weight Src inhibitors in animal models of osteoporosis. At the
Obesity does not aggravate osteoporosis or osteoblastic insulin resistance in orchiectomized rats.
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The present study aimed to test the hypothesis that testosterone deprivation impairs osteoblastic insulin signaling, decreases osteoblast survival, reduces bone density, and that obesity aggravates those deleterious effects in testosterone-deprived rats. Twenty four male Wistar rats underwent either
Future developments in osteoporosis therapy.
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Anti-resorptives that prevent osteoclasts from resorbing bone are the mainstay of treatment for osteoporosis, while parathyroid hormone is the only agent available that stimulates osteoblasts to form bone. Advances in knowledge about metabolic pathways in bone cell biology have identified specific
Fluoride increases tyrosine kinase activity in osteoblast-like cells: regulatory role for the stimulation of cell proliferation and Pi transport across the plasma membrane.
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Fluoride is one of the most effective agents for the treatment of vertebral osteoporosis because of its ability to increase osteoblast proliferation. The present study further investigates the role of protein tyrosine phosphorylation previously suggested to mediate the mitogenic effect of fluoride
Alendronate inhibition of protein-tyrosine-phosphatase-meg1.
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Alendronate (4-amino-1-hydroxybutylidene-1,1-bisphosphonate) is a potent bisphosphonate that inhibits osteoclastic bone resorption and has proven effective for the treatment of osteoporosis. Its molecular mechanism of action, however, has not been defined precisely. Here we report that alendronate
How does alendronate inhibit protein-tyrosine phosphatases?
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Alendronate (4-amino-1-hydroxybutylidene 1,1-bisphosphonate) is a drug used in the treatment of osteoporosis and other bone diseases. The inhibition of protein-tyrosine phosphatases (PTPs) by alendronate suggests that PTPs may be molecular targets. As a clear understanding of the inhibition
Structural basis of Src tyrosine kinase inhibition with a new class of potent and selective trisubstituted purine-based compounds.
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The tyrosine kinase pp60src (Src) is the prototypical member of a family of proteins that participate in a broad array of cellular signal transduction processes, including cell growth, differentiation, survival, adhesion, and migration. Abnormal Src family kinase (SFK) signaling has been linked to
Insulin sensitization by a novel partial peroxisome proliferator-activated receptor γ agonist with protein tyrosine phosphatase 1B inhibitory activity in experimental osteoporotic rats.
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The pharmacological profile of (S)-7-(2-{2-[(E)-2-cyclopentylvinyl]-5-methyloxazol-4-yl}-ethoxy)-2-[(2E,4E)-hexadienoyl]-1,2,3,4-tetrahydroisoquinoline-3-carboxylic acid (KY-201), a peroxisome proliferator-activated receptor (PPAR) γ agonist, was compared with that of rosiglitazone in ovariectomized
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