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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >Heme oxygenase 1 expression induced by IL-10 requires STAT-3 and phosphoinositol-3 kinase and is inhibited by lipopolysaccharide.
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Heme oxygenase 1 expression induced by IL-10 requires STAT-3 and phosphoinositol-3 kinase and is inhibited by lipopolysaccharide.

机译:IL-10诱导的血红素加氧酶1表达需要STAT-3和磷酸肌醇3激酶,并被脂多糖抑制。

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摘要

Heme-oxygenase 1 (HO-1) is a stress-response protein with anti-inflammatory activity. This study has examined the regulation of HO-1 expression by the anti-inflammatory factor, interleukin (IL)-10 and whether HO-1 could account for the function of the cytokine. IL-10-induced expression of HO-1 required the activation of signal transducer and activator of transcription (STAT)-3 but not p38 mitogen-activated protein kinase. However, expression of HO-1 also required the activation of the phosphatidylinositol-3 kinase pathway, a signaling mechanism not required for the anti-inflammatory activity of IL-10. Moreover, induction of HO-1 expression was not restricted to IL-10, as IL-6, a cytokine known to activate STAT-3, could also induce the protein. In human macrophages, lipopolysaccharide inhibited HO-1 expression induced by IL-10. Also, inhibition of HO-1 activity by the specific inhibitor zinc-II-protoporphyrin-IX had no effect on the anti-inflammatory function of IL-10. In summary, although IL-10 does regulate HO-1 expression, it does not appear to play a significant role in the anti-inflammatory activity of the cytokine.
机译:血红素加氧酶1(HO-1)是一种具有抗炎活性的应激反应蛋白。这项研究检查了抗炎因子白介素(IL)-10对HO-1表达的调节作用,以及HO-1是否可以解释细胞因子的功能。 IL-10诱导的HO-1表达需要激活信号转导子和转录激活子(STAT)-3,但不需要p38丝裂原激活的蛋白激酶。但是,HO-1的表达还需要激活磷脂酰肌醇3激酶途径,这是IL-10抗炎活性所不需要的信号传导机制。此外,HO-1表达的诱导不仅限于IL-10,因为IL-6(一种已知可激活STAT-3的细胞因子)也可以诱导该蛋白。在人类巨噬细胞中,脂多糖抑制IL-10诱导的HO-1表达。同样,特异性抑制剂锌-II-原卟啉-IX对HO-1活性的抑制对IL-10的抗炎功能没有影响。总之,尽管IL-10确实调节HO-1的表达,但它似乎在细胞因子的抗炎活性中没有发挥重要作用。

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