Abstract

We recently reported that Thy-1, a surface molecule induced on the rat endothelium, regulates vascular permeability at sites of inflammation. Although the rat inferior vena cava (IVC) did not express Thy-1in vivo, cultured endothelial cells from the IVC did express Thy-1, thereby suggesting that the expression was acquired during cultivation of the cellsin vitro,possibly by autoactivation by cytokine-like substances. Interleukin (IL)-1α but not tumor necrosis factor (TNF)-α or interferon (IFN)-γ was detected in culture supernatants of rat endothelial cells (REC) by ELISA. The production of IL-1α by REC was augmented by exogenously added IL-1α, thereby implying the presence of autocrine regulation by IL-1α. The unaltered expression of Thy-1 by exogenously added IL-1α suggests that Thy-1 expression on REC had already been maximally induced by autologous cytokines; the expression of Thy-1 on REC was lowered by inhibiting protein kinase C and by depleting IL-1α activity from culture supernatants. Although cytokine-like regulators, other than IL-1α, TNF-α, or IFN-γ, produced by REC may also modulate the expression of Thy-1, it is at least in part mediated by IL-1αin vitro.Moreover, Thy-1 expression was induced on rat vascular endothelium at the subcutis where recombinant IL-1α was injected. The evidence indicates that IL-1α functions as one regulator responsible for the induction of Thy-1 on REC,in vitroas well asin vivo.

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