抵抗素上调人内皮细胞中趋化因子的表达：与肿瘤坏死因子-α无叠加效应。
Resistin up-regulates fractalkine expression in human endothelial cells: lack of additive effect with TNF-alpha.
作者信息
Manduteanu Ileana, Dragomir Elena, Calin Manuela, Pirvulescu Monica, Gan Ana Maria, Stan Daniela, Simionescu Maya
机构信息
Institute of Cellular Biology and Pathology Nicolae Simionescu, 8 B.P. Hasdeu Street, P.O. Box 35-14, 050568 Bucharest, Romania.
出版信息
Biochem Biophys Res Commun. 2009 Mar 27;381(1):96-101. doi: 10.1016/j.bbrc.2009.02.015. Epub 2009 Feb 11.
Resistin is a cytokine and fractalkine (Fk) a cell adhesion molecule and chemokine that contribute to human vascular inflammation by mechanisms not clearly defined. We questioned whether resistin induces Fk expression in human endothelial cells (HEC), compared the effect with that of the pro-inflammatory cytokine, TNF-alpha, and evaluated the consequences of co-stimulating HEC with both activators on Fk induction and on the signalling molecules involved. We found that resistin up-regulated Fk expression at comparable level to that of TNF-alpha by a mechanism involving P38 and JNK MAPK and NF-kappaB. Co-stimulation of cells with resistin and TNF-alpha did not increase Fk expression induced by every single inducer. Moreover resistin reduced the expression induced by TNF-alpha in HEC. The new data uncover Fk as a novel molecular link between resistin and inflammation and show that resistin and TNF-alpha have no additive effect in Fk up-regulation or on the signalling molecules implicated.
抵抗素是一种细胞因子，而 fractalkine（Fk）是一种细胞黏附分子和趋化因子，它们通过尚未明确的机制促成人类血管炎症。我们探讨了抵抗素是否会诱导人内皮细胞（HEC）中 Fk 的表达，将其作用效果与促炎细胞因子肿瘤坏死因子-α（TNF-α）进行比较，并评估同时用这两种激活剂刺激 HEC 对 Fk 诱导及相关信号分子的影响。我们发现，抵抗素通过涉及 P38 和 JNK 丝裂原活化蛋白激酶（MAPK）以及核因子-κB（NF-κB）的机制，将 Fk 表达上调至与 TNF-α相当的水平。用抵抗素和 TNF-α共同刺激细胞并不会增加单一诱导剂所诱导的 Fk 表达。此外，抵抗素会降低 TNF-α在 HEC 中所诱导的表达。这些新数据揭示 Fk 是抵抗素与炎症之间的一种新型分子联系，并表明抵抗素和 TNF-α在 Fk 上调或相关信号分子方面没有相加作用。
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