Journal
BIOMEDICAL RESEARCH-TOKYO
Volume 31, Issue 5, Pages 281-286Publisher
BIOMEDICAL RESEARCH PRESS LTD
DOI: 10.2220/biomedres.31.281
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Several studies have demonstrated the association of plasminogen activator inhibitor-1 (PAI-1) with osteonecrosis, but the underlying mechanism of osteonecrosis and its relationship with local PAI-1 is not clear. The objective of this study was to evaluate PAI-1 production by primary human bone marrow adipocytes and the effects of glucocorticoid administration. Bone marrow was obtained from 25 individuals during prosthetic insertion. Mature adipocytes were cultured for 24 h with or without dexamethasone. PAI-1, adiponectin, tumor necrosing factor-alpha (TNF alpha) expression were measured by latex photometric immunoassay or RT-PCR. Adiponectin, TNF alpha and PAI-1 were detected in all culture media. PAI-1 expression was significantly increased by treatment with 10(-6) mol/L dexamethasone up to 24 h in protein and mRNA levels, while the levels of other adipokines did not change by dexamethasone. These results suggest that bone marrow adipocytes may play important roles for the development of glucocorticoid-induced osteonecrotic diseases by enhancing PAI-1 expression.
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