## Abstract Inflammatory bowel diseases (IBD) are linked to an increased risk of developing colon cancer, by inflammatory mediators and alterations to the extracellular matrix (ECM). The events induced by inflammatory mediators lead to dysregulated activation and induction of inflammatory genes suc
Interleukin-1α induces cyclooxygenase-2 expression in bone-derived endothelial cells
✍ Scribed by Takumi Nakagawa; Naoya Fujita; Tomoko Oh-Hara; Takahide Kurokawa; Kozo Nakamura; Takashi Tsuruo
- Publisher
- John Wiley and Sons
- Year
- 1999
- Tongue
- English
- Weight
- 144 KB
- Volume
- 179
- Category
- Article
- ISSN
- 0021-9541
No coin nor oath required. For personal study only.
✦ Synopsis
Histological studies have suggested that vascular endothelial cells in bone are members of a complex network that regulates bone development and remodeling by producing soluble factors or by mediating cell-cell adhesion. To clarify the role of bone-derived endothelial cell lines (BDECs) in bone remodeling, we established several clones of BDECs from the femurs of BALB/c mice after transformation with the SV40 virus. Then we examined the response of these clones to interleukin-1␣ (IL-1␣). IL-1␣ is known to induce bone resorption in part by increasing the expression of cyclooxygenase-2 (COX-2) that is associated with the production of PGE 2 in osteoblast-lineage cells. Treating the primary and established BDECs with IL-1␣ induced COX-2 mRNA expression. A transcriptional activation assay revealed that the treatment with IL-1␣ increased COX-2 promoter activity in a dose-dependent manner, and IL-1␣ promoted COX-2 protein expression in BDECs. Treatment with IL-1␣ promoted PGE 2 production from BDECs in a dose-dependent manner. These results indicate that IL-1␣ stimulates PGE 2 synthesis largely by inducing BDECs to express COX-2. Because PGE 2 stimulates bone resorption, these vascular endothelial cells, as well as osteoblast cells, play important roles in bone remodeling.
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