Ishizu A, Ishikura H, Nakamaru Y, Kikuchi K, Koike T, Yoshiki T
Department of Pathology, Hokkaido University School of Medicine, Kita-15, Nishi-7, Kita-ku, Sapporo, 060, Japan.
Microvasc Res. 1997 Jan;53(1):73-8. doi: 10.1006/mvre.1996.1986.
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-1 in vivo, cultured endothelial cells from the IVC did express Thy-1, thereby suggesting that the expression was acquired during cultivation of the cells in vitro, possibly by autoactivation by cytokine-like substances. Interleukin (IL)-1alpha but not tumor necrosis factor (TNF)-alpha or interferon (IFN)-gamma was detected in culture supernatants of rat endothelial cells (REC) by ELISA. The production of IL-1alpha by REC was augmented by exogenously added IL-1alpha, thereby implying the presence of autocrine regulation by IL-1alpha. The unaltered expression of Thy-1 by exogenously added IL-1alpha 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-1alpha activity from culture supernatants. Although cytokine-like regulators, other than IL-1alpha, TNF-alpha, or IFN-gamma, produced by REC may also modulate the expression of Thy-1, it is at least in part mediated by IL-1alpha in vitro. Moreover, Thy-1 expression was induced on rat vascular endothelium at the subcutis where recombinant IL-1alpha was injected. The evidence indicates that IL-1alpha functions as one regulator responsible for the induction of Thy-1 on REC, in vitro as well as in vivo.
我们最近报道，Thy-1是一种在大鼠内皮细胞上诱导产生的表面分子，可调节炎症部位的血管通透性。尽管大鼠下腔静脉（IVC）在体内不表达Thy-1，但来自IVC的培养内皮细胞确实表达Thy-1，这表明该表达是在细胞体外培养过程中获得的，可能是通过细胞因子样物质的自激活作用。通过ELISA在大鼠内皮细胞（REC）的培养上清液中检测到白细胞介素（IL）-1α，但未检测到肿瘤坏死因子（TNF）-α或干扰素（IFN）-γ。外源性添加IL-1α可增强REC产生IL-1α，这意味着存在IL-1α的自分泌调节。外源性添加IL-1α后Thy-1表达未改变，表明REC上的Thy-1表达已经被自体细胞因子最大程度地诱导；抑制蛋白激酶C并从培养上清液中去除IL-1α活性可降低REC上Thy-1的表达。尽管REC产生的除IL-1α、TNF-α或IFN-γ之外的细胞因子样调节剂也可能调节Thy-1的表达，但至少在体外部分是由IL-1α介导的。此外，在皮下注射重组IL-1α的部位，大鼠血管内皮细胞上诱导出了Thy-1表达。证据表明，IL-1α在体外和体内均作为诱导REC上Thy-1表达的一种调节因子发挥作用。
