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Basic fibroblast growth factor induces cyclooxygenase-2 expression in endothelial cells derived from bone
1Institute of Molecular and Cellular Biosciences, University of Tokyo, 1-1-1, Yayoi, Tokyo, Bunkyo-ku, 113-0032, Japan.
Biochemical and Biophysical Research Communications
|January 28, 1999
Summary
Bone endothelial cells (BDECs) control bone remodeling by regulating prostaglandin E2 (PGE2) production. Basic fibroblast growth factor (bFGF) stimulates BDECs to express cyclooxygenase-2 (COX-2), increasing PGE2, which influences bone resorption and osteoclast formation.
Area of Science:
- Bone biology
- Cellular and molecular biology
- Endocrinology
Background:
- Histological studies suggest a role for bone endothelial cells (BDECs) in osteolytic bone diseases.
- The precise contribution of BDECs to bone remodeling remains incompletely understood.
Purpose of the Study:
- To investigate the response of BDECs to basic fibroblast growth factor (bFGF).
- To elucidate the mechanism by which BDECs influence bone remodeling.
Main Methods:
- Primary and cloned murine BDECs were isolated from BALB/c mouse femurs.
- BDECs were treated with bFGF, and cyclooxygenase-2 (COX-2) mRNA and protein expression were analyzed.
- Prostaglandin E2 (PGE2) production was measured and its regulation by COX-2 was assessed using inhibitors and antisense oligodeoxynucleotides.
Main Results:
- bFGF treatment induced COX-2 mRNA and protein expression in BDECs.
- bFGF significantly promoted PGE2 production in a COX-2-dependent manner.
- Inhibition of COX-2 suppressed bFGF-induced PGE2 secretion.
Conclusions:
- Bone endothelial cells contribute to bone remodeling through the control of COX-2 expression.
- bFGF-induced COX-2 expression in BDECs leads to increased PGE2 production, a key mediator of bone resorption and osteoclastogenesis.