Tumor necrosis factor receptor family member RANK mediates osteoclast differentiation and activation induced by osteoprotegerin ligand.
نویسندگان
چکیده
A receptor that mediates osteoprotegerin ligand (OPGL)-induced osteoclast differentiation and activation has been identified via genomic analysis of a primary osteoclast precursor cell cDNA library and is identical to the tumor necrosis factor receptor (TNFR) family member RANK. The RANK mRNA was highly expressed by isolated bone marrow-derived osteoclast progenitors and by mature osteoclasts in vivo. Recombinant OPGL binds specifically to RANK expressed by transfected cell lines and purified osteoclast progenitors. Transgenic mice expressing a soluble RANK-Fc fusion protein have severe osteopetrosis because of a reduction in osteoclasts, similar to OPG transgenic mice. Recombinant RANK-Fc binds with high affinity to OPGL in vitro and blocks osteoclast differentiation and activation in vitro and in vivo. Furthermore, polyclonal Ab against the RANK extracellular domain promotes osteoclastogenesis in bone marrow cultures suggesting that RANK activation mediates the effects of OPGL on the osteoclast pathway. These data indicate that OPGL-induced osteoclastogenesis is directly mediated through RANK on osteoclast precursor cells.
منابع مشابه
The role of TNF-receptor family members and other TRAF-dependent receptors in bone resorption
The contribution of osteoclasts to the process of bone loss in inflammatory arthritis has recently been demonstrated. Studies in osteoclast biology have led to the identification of factors responsible for the differentiation and activation of osteoclasts, the most important of which is the receptor activator of NF-kappa B ligand/osteoclast differentiation factor (RANKL/ODF), a tumor necrosis f...
متن کاملTRANCE is a TNF family member that regulates dendritic cell and osteoclast function.
Tumor necrosis factor (TNF)-related activation-induced cytokine (TRANCE) is a new member of the TNF family emerging as a key regulator of the immune system and of bone development and homeostasis. TRANCE is expressed on activated T cells and activates mature dendritic cells (DC), suggesting that it plays a role in the T cell-DC interaction during an immune response. Furthermore, TRANCE is expre...
متن کاملBone loss: Factors that regulate osteoclast differentiation - an update
Osteoclast activation is a critical cellular process for pathological bone resorption, such as erosions in rheumatoid arthritis (RA) or generalized bone loss. Among many factors triggering excessive osteoclast activity, cytokines such as IL-1 or tumour necrosis factor (TNF)-alpha play a central role. New members of the TNF receptor ligand family (namely receptor activator of nuclear factor-kapp...
متن کاملPathophysiology of RANK ligand (RANKL) and osteoprotegerin (OPG).
Receptor activator of nuclear factorκ B ligand (RANKL) is a membrane-bound peptide of the tumor necrosis factor (TNF) ligand superfamily [14]. Rich sources of RANKL expression include T lymphocytes [12] and osteoblastic lineage cells [8]. In the presence of permissive concentrations of macrophage-colony stimulating factor (M-CSF), RANKL stimulates the differentiation, proliferation, fusion and ...
متن کاملUmbilical cord and maternal plasma thiol concentrations in normal pregnancy.
Estrogen stimulates gene expression and protein production of osteoprote-gerin by human osteoblastic cells. Osteoprotegerin ligand is a cytokine that regulates osteoclast differentiation and activation. Immunological characterization of circulating osteoprotegerin/osteoclasto-genesis inhibitory factor: increased serum concentrations in postmeno-pausal women with osteoporosis. Osteoprotegerin an...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Proceedings of the National Academy of Sciences of the United States of America
دوره 96 7 شماره
صفحات -
تاریخ انتشار 1999