Articles tagged with Osteoclasts
Researchers at the Weizmann Institute of Science have discovered that the impermeable ring formed by osteoclasts is composed of individual podosomes held together by protein filaments. This unique structure allows the cells to confine bone-eating acids and enzymes, enabling efficient bone digestion.
Cortisone has been found to weaken bones by targeting osteoclasts, which dismantle old bone. Researchers may now be able to develop therapeutic targets to prevent cortisone's damaging side effects on bone.
Researchers reveal that glucocorticoids, commonly used for inflammatory disorders, can cause osteoporosis by delaying osteoclast death and suppressing bone formation. Prolonged GC use affects bone health in mice with normal and disrupted GC receptors.
The inner walls of bones serve as sites for both bone breakdown and reconstruction, with osteoclasts playing a crucial role in releasing hematopoietic stem cells. This process is essential for maintaining balance in the body's response to injury or inflammation, and may have implications for bone marrow transplant techniques.
Dr. Teitelbaum's research reveals that blocking integrin receptors on osteoclasts can prevent bone loss in osteoporosis and rheumatoid arthritis, offering new drug targets. Additionally, his work has shed light on the effects of protease inhibitors on osteoclasts in HIV/AIDS patients.
Scientists discovered that interleukin-6 increases in TM patients' cerebrospinal fluid and is linked to tissue injury. Arsenic trioxide inhibits nuclear receptor function via SEK1/JNK-mediated RXR phosphorylation. Epithelial myosin light chain kinase-dependent barrier dysfunction mediates T cell activation-induced diarrhea.
Researchers at Yale University identified IRAK-M as a key regulator of bone cells, finding that its presence prevents bone loss and its absence leads to severe osteoporosis in mice. The study suggests IRAK-M could be a new target for treating or preventing osteoporosis.
A major axis within bone cells regulates bone production and loss, providing a potential new target for treating debilitating osteoporosis. Local regulation of bone mass is now believed to occur primarily in the bone, not in the brain as previously thought.
A study published in the Journal of Clinical Investigation reveals that M-CSF and alphaV beta3 integrin collaborate to regulate osteoclast differentiation. The discovery brings scientists closer to understanding the mechanisms behind osteoporosis, a condition affecting 50% of Caucasian and Asian women after age 65.
Researchers discover two compounds that inhibit parathyroid hormone-related protein production in human breast cancer cells, reducing metastatic bone breakdown and calcium levels. The findings suggest a novel therapeutic approach to treating bone metastasis and hypercalcemia in breast cancer patients.
Researchers created mice lacking SHIP gene to understand how bone forms and breaks down in diseases like JPD. The study reveals that mice with deficient SHIP develop osteoclasts similar to those found in humans with JPD, leading to severely osteoporotic conditions.
Researchers at Washington University in St. Louis discovered that blood vessels signal the onset of bone loss in diseases such as rheumatoid arthritis and osteoporosis. The discovery sheds light on how inflamed blood vessels trigger a cascade of events leading to local bone destruction.
Researchers found that alcohol feeding impaired osteoblast function and led to increased bone turnover, contributing to bone fragility. In contrast, mice lacking the interleukin-6 (IL-6) gene had better maintained bone mass and reduced fractures.
Researchers found that high concentrations of nitric oxide in osteoclasts prevent excessive bone resorption, a process linked to diseases like osteoporosis. This discovery may lead to new strategies for preventing bone loss and potentially treating inflammatory conditions.