A mutual antagonism exists between interleukin-Is (IL-Is) as pro-inflammatory and glucocorticoids as anti-inflammatory mediators. This report examines the effects of IL-1 on the induction by dexamethasone of alkaline phosphatase in LEI1 murine endothelial cells. Dexamethasone increases the specific
Regulation of expression of the cell adhesion receptors, integrins, by recombinant human interleukin-1β in human osteosarcoma cells: Inhibition of cell proliferation and stimulation of alkaline phosphatase activity
✍ Scribed by Shoukat Dedhar
- Publisher
- John Wiley and Sons
- Year
- 1989
- Tongue
- English
- Weight
- 1016 KB
- Volume
- 138
- Category
- Article
- ISSN
- 0021-9541
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✦ Synopsis
Recombinant human interleukin-1 beta, a mediator of osteoblastic cell function, was found to regulate the expression of the cell adhesion receptors, integrins, on human osteosarcoma cells. Interleukin-1 beta (IL-1 beta) at picomolar concentrations, specifically elevated approximately six- to tenfold the expression of the beta 1 subunit and its associated alpha subunits, but not the related vitronectin receptor, within 20 hours. Integrin beta 1 messenger RNA levels were elevated within 6 hours and peaked to tenfold higher levels after 20 hours exposure to IL-1 beta in two human osteosarcoma cell lines. The increase in the cell-surface beta 1 integrins resulted in a stronger binding of the IL-1 beta-treated cells to fibronectin. Cell growth was also inhibited by IL-1 beta, cell morphology was altered, and IL-1 beta-treated cells expressed an approximately two- to threefold higher alkaline phosphatase. This increase in alkaline phosphatase activity was found to be independent of the inhibition of cell proliferation. These data indicate that the beta 1 integrin family of cell surface receptors is a target for regulation by IL-1 beta, which also regulates cell proliferation and the expression of the osteoblastic phenotype in human osteosarcoma cells.
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