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Ninjurin1 positively regulates osteoclast development by enhancing the survival of prefusion osteoclasts
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Ninjurin1 positively regulates osteoclast development by enhancing the survival of prefusion osteoclasts
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Journal Article
Ninjurin1 positively regulates osteoclast development by enhancing the survival of prefusion osteoclasts
2019
Overview
Osteoclasts (OCs) are bone-resorbing cells that originate from hematopoietic stem cells and develop through the fusion of mononuclear myeloid precursors. Dysregulation of OC development causes bone disorders such as osteopetrosis, osteoporosis, and rheumatoid arthritis. Although the molecular mechanisms underlying osteoclastogenesis have been well established, the means by which OCs maintain their survival during OC development remain unknown. We found that Ninjurin1 (Ninj1) expression is dynamically regulated during osteoclastogenesis and that
Ninj1
−/−
mice exhibit increased trabecular bone volume owing to impaired OC development. Ninj1 deficiency did not alter OC differentiation, transmigration, fusion, or actin ring formation but increased Caspase-9-dependent intrinsic apoptosis in prefusion OCs (preOCs). Overexpression of Ninj1 enhanced the survival of mouse macrophage/preOC RAW264.7 cells in osteoclastogenic culture, suggesting that Ninj1 is important for the survival of preOCs. Finally, analysis of publicly available microarray data sets revealed a potent correlation between high
NINJ1
expression and destructive bone disorders in humans. Our data indicate that Ninj1 plays an important role in bone homeostasis by enhancing the survival of preOCs.
Bone development: Regulating the remodelers
A protein called ninjurin1 regulates the activity of bone-degrading osteoclast cells, and may play an important role in various skeletal degenerative disorders. Normal skeletal development requires careful coordination by bone-building osteoblasts and by osteoclasts, which break down and remodel bone. Researchers led by Kyu-Won Kim of Seoul National University in South Korea have shown that ninjurin1 regulates both the development and survival of osteoclasts. They generated genetically modified mice that lack this protein, and observed notable skeletal defects, including abnormal accumulation of bone mass in long bones such as the femur. Elevated ninjurin1 levels are a feature of conditions such as osteoporosis and rheumatoid arthritis, and the researchers propose that therapeutic agents that target this molecule could help control the bone damage caused by improperly regulated osteoclasts.
Publisher
Nature Publishing Group UK,Springer Nature B.V,Nature Publishing Group,생화학분자생물학회
Subject
/ 13/31
/ 14/19
/ 14/35
/ 38/61
/ 64/60
/ 82/80
/ Actin
/ Animals
/ Biomedical and Life Sciences
/ Cancellous Bone - growth & development
/ Cancellous Bone - metabolism
/ Caspase
/ Cell Adhesion Molecules, Neuronal - genetics
/ Cell Adhesion Molecules, Neuronal - metabolism
/ Femur
/ Humans
/ Male
/ Mice
/ Nerve Growth Factors - genetics
/ Nerve Growth Factors - metabolism
/ 생화학
