These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Synthesis of osteoprotegerin and RANKL by megakaryocytes is modulated by oestrogen. Author: Bord S, Frith E, Ireland DC, Scott MA, Craig JI, Compston JE. Journal: Br J Haematol; 2004 Jul; 126(2):244-51. PubMed ID: 15238146. Abstract: To investigate the mechanisms by which megakaryocytes (MKs) may influence bone remodelling, CD34(+) cells were cultured for 6, 9 and 12 d with or without 17beta-oestradiol (E) and immunolocalized for osteoprotegerin (OPG), receptor activator of nuclear factor (NF)-kappaB ligand (RANKL) and CD61. Specific protein expression was measured quantitatively by image analysis. Fluorescence-based immunocytochemistry was used to co-localize OPG and RANKL with CD61. OPG and RANKL mRNA was assessed in CD61(+) cells with or without E at 24 and 48 h. At 6 d, OPG and RANKL expression was unchanged by E treatment. At 9 d, the E-treated cultures with maturing MKs showed a 1.72-fold (P < 0.01) increase in OPG expression and a 1.8-fold (P < 0.01) reduction in RANKL. Maximal OPG expression was seen at 12 d with a threefold induction of expression (P < 0.001), whilst RANKL levels were further suppressed by 2.3-fold compared with controls (P < 0.001). CD61 co-localized with OPG and RANKL. mRNA data were consistent with that of protein, with a 90-fold induction in OPG expression and a 34-fold suppression of RANKL expression by E (P < 0.001). Thus, E stimulates megakaryocytopoiesis and modulates OPG and RANKL expression, providing evidence that MKs may play a role in bone remodelling and, in particular, in E-induced changes in osteoclastogenesis and bone resorption.[Abstract] [Full Text] [Related] [New Search]