Does OPG bind to rank or RANKL?

Does OPG bind to rank or RANKL?

Osteoprotegerin (OPG) is secreted by osteoblasts and osteogenic stromal stem cells and protects the skeleton from excessive bone resorption by binding to RANKL and preventing it from interacting with RANK. The RANKL/OPG ratio in bone marrow is thus an important determinant of bone mass in normal and disease states.

Where is RANKL found?

High protein expression of RANKL is commonly detected in the lungs, thymus and lymph nodes. Low protein expression is found in bone marrow, the stomach, peripheral blood, the spleen, the placenta, leukocytes, the heart, the thyroid, and skeletal muscle.

What is OPG in osteoporosis?

OPG deficiency causes osteoporosis in mice, and, when administered to ovariectomized rats, OPG decreases osteoclast activity and restores normal bone mass. OPG is produced by osteoblasts and arterial cells, and inhibits osteoclast function by neutralizing receptor activator of NF-kappa B ligand (RANKL).

What does OPG bind to?

OPG binds to syndecan-1 on the surface of normal and multiple myeloma plasma cells to be internalised and degraded. However the overabundance of proliferating myeloma cells results in the excessive binding and inhibition of OPG by syndecan-1.

What causes the RANKL?

In inflammatory conditions, such as rheumatoid arthritis, the numbers of immune and accessory cells are increased in affected joints. Some of these cells produce RANKL in response to locally elevated levels of pro-inflammatory cytokines and other inflammatory mediators.

What is OPG in bone remodeling?

OPG protects bone from excessive resorption by binding to RANKL and preventing it from binding to RANK. Thus, the relative concentration of RANKL and OPG in bone is a major determinant of bone mass and strength.

What is RANK Ligand inhibitor?

It is a receptor activator of nuclear factor-κB ligand (RANKL) inhibitor, which binds to and inhibits osteoblast-produced RANKL, in turn reduces the binding between RANKL and osteoclast receptor RANK, therefore decreases osteoclast-mediated bone resorption and turnover.