Sclerostin, an osteocyte-expressed negative regulator of bone formation, is one of the inhibitors of Wnt signalling which is a critical pathway in the correct process of osteoblast differentiation. It has been demonstrated that Wnt signalling through the secretion of Wnt inhibitors, such as DKK1, sFRP-2 and - 3, plays a key role in the decreased osteoblast activity associated with multiple myeloma (MM) bone disease. We provide evidence that sclerostin is expressed by myeloma cells, that are human myeloma cell lines (HMCLs) and plasma cells (CD138+ cells) obtained from the bone marrow of a large number of MM patients with bone disease. Moreover, we show that there are no differences in sclerostin serum levels between MM patients and controls. Thus, our data indicate that MM cells, as sclerostin source in the bone marrow, could create a microenvironment with high sclerostin concentration, that could contribute in inhibiting osteoblast differentiation.
Sclerostin is overexpressed by plasma cells from multiple myeloma patients
MORI, GIORGIO;
2011-01-01
Abstract
Sclerostin, an osteocyte-expressed negative regulator of bone formation, is one of the inhibitors of Wnt signalling which is a critical pathway in the correct process of osteoblast differentiation. It has been demonstrated that Wnt signalling through the secretion of Wnt inhibitors, such as DKK1, sFRP-2 and - 3, plays a key role in the decreased osteoblast activity associated with multiple myeloma (MM) bone disease. We provide evidence that sclerostin is expressed by myeloma cells, that are human myeloma cell lines (HMCLs) and plasma cells (CD138+ cells) obtained from the bone marrow of a large number of MM patients with bone disease. Moreover, we show that there are no differences in sclerostin serum levels between MM patients and controls. Thus, our data indicate that MM cells, as sclerostin source in the bone marrow, could create a microenvironment with high sclerostin concentration, that could contribute in inhibiting osteoblast differentiation.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.