نتایج جستجو برای: rankl
تعداد نتایج: 3831 فیلتر نتایج به سال:
Vascular calcification commonly associated with several pathologies and it has been suggested to be similar to bone mineralization. The axis RANKL-OPG (receptor activator of nuclear factor kappaB ligand-osteoprotegerin) finely controls bone turnover. RANKL has been suggested to increase vascular calcification, but direct evidence is missing. Thus, in the present work, we assess the effect of RA...
OBJECTIVE Clinical and experimental studies demonstrate the important roles of vascular smooth muscle cells (VSMC) in the pathogenesis of atherosclerosis. We have previously determined that the osteogenic transcription factor Runx2 is essential for VSMC calcification. The present study characterized Runx2-regulated signals and their potential roles in vascular calcification. METHODS AND RESUL...
OBJECTIVE Osteoprotegerin (OPG) and its ligand 'receptor activator of NF-kB ligand' (RANKL) are important regulators of bone metabolism. RANKL, expressed in osteoblasts, activates osteoclast differentiation and osteoclast function by binding the 'receptor activator of NF-kB' (RANK), expressed in ostoclast precursors and mature osteoclasts. The effect is prevented by OPG, a soluble receptor of R...
Receptor activator of NF-kappaB ligand (RANKL) is an essential mediator of osteoclast formation, function, and survival. The effects of RANKL are inhibited by a soluble decoy receptor called osteoprotegerin (OPG). Total ablation of RANKL in knockout mice leads to high bone mass, lymph node agenesis, and altered lymphocyte differentiation. In contrast, RANKL inhibition via OPG suppresses bone re...
مولتیپل میلوما یک بیماری خونی است که با تکثیر پلاسماسل های بدخیم در مغز استخوان همراه است.عدم تعادل بین فعالیت استئوبلاست و استئوکلاست موجب شکستگی های پاتولوژیکی استخوان، علائم عصبی(درد) و افزایش کلسیم خون می گردد. به تازگی اختلال در سیستم opg، rankl و rank به عنوان مکانیسم دیگری برای فعالیت استئوکلاست ها و در نهایت تخریب استخوان مطرح شده است.در مطالعات قبلی نشان داده شد پلاسماسل های جدا شده از...
Tartrate-resistant acid phosphatase (TRAP) plays an important role in bone resorption. TRAP expression in osteoclasts is regulated by receptor activator of NF-kappaB (RANKL), a potent activator of osteoclast differentiation. However, the molecular mechanism underlying the RANKL-induced TRAP expression remains unknown. Here we show that two regions in the mouse TRAP promoter (one at -1858 to -12...
Although receptor activator of nuclear factor (NF)-kappaB ligand (RANKL) signaling has been shown to prolong the survival of mature dendritic cells (DCs), the association of RANKL pathway with Fas-mediated apoptosis is obscure. Here, we found that bone marrow-derived DCs (BMDCs) from the Fas-deficient strain MRL/lpr mice, could survive much longer than normal DCs. The expressions of Bcl-x and B...
STUDY DESIGN Experimental animal study. PURPOSE To evaluate pain-related behavior and changes in nuclear factor-kappa B (NF-kB), receptor activator of NF-kB (RANK), and ligand (RANKL) in dorsal root ganglia (DRG) after combined sciatic nerve compression and nucleus pulposus (NP) application in rats. OVERVIEW OF LITERATURE The pathological mechanisms underlying pain from lumbar-disc herniati...
During bone resorption, osteoclasts are exposed to high Ca2+ concentrations (up to 40 mM). The role of high extracellular Ca2+ in receptor activator of NF-kappaB ligand (RANKL)-mediated osteoclast survival and their functional interrelationship is unclear. In this study, we show that RANKL enhances osteoclast tolerance to high extracellular Ca2+ by protecting the cell from cell death in a dose ...
Osteoblasts express two key molecules for osteoclast differentiation, receptor activator of NF-κB ligand (RANKL) and osteoprotegerin (OPG), a soluble decoy receptor for RANKL. RANKL induces osteoclastogenesis, while OPG inhibits it by blocking the binding of RANKL to RANK, a cellular receptor of RANKL. OPG-deficient (OPG-/-) mice exhibit severe alveolar bone loss with enhanced bone resorption. ...
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