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首页> 外文期刊>Cell and Tissue Research >Beta-arrestin 1 is involved in the catabolic response stimulated by hyaluronan degradation in mouse chondrocytes
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Beta-arrestin 1 is involved in the catabolic response stimulated by hyaluronan degradation in mouse chondrocytes

机译：β-arrestin1参与小鼠软骨细胞中透明质酸降解刺激的分解代谢反应

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摘要

Beta-arrestin-1 (beta-arrestin-1) is an adaptor protein that functions in the termination of G-protein activation and seems to be involved in the mediation of the inflammatory response. Interleukin-1 beta (IL-1 beta) elicits the expression of inflammatory mediators through a mechanism involving hyaluronan (HA) degradation, thereby contributing to toll-like receptor 4 (TLR-4) and CD44 activation. Stimulation of both receptors induces nuclear factor kappaB (NF-kB) activation that, through transforming-growth-factor-activated-kinase-1 (TAK-1), in turn stimulates the inflammatory mediators of transcription. As beta-arrestin-1 seems to play an inflammatory role in arthritis, we have investigated the involvement of beta-arrestin-1 in a model of IL-1 beta-induced inflammatory response in mouse chondrocytes. IL-1 beta treatment significantly increases chondrocytes TLR-4, CD44, beta-arrestin-1, TAK-1, and serine/threonine kinase (AKT) mRNA expression and related protein levels. NF-kB is also markedly activated with consequent tumor-necrosis-factor-alpha, interleukin-6, and inducible-nitric-oxide-synthase up-regulation. Treatment of IL-1 beta-stimulated chondrocytes with beta-arrestin-1 and/or AKT and/or TAK-1-specific inhibitors significantly reduces all parameters, although the inhibitory effect exerted by TAK-1-mediated pathways is more effective than that of beta-arrestin-1. beta-Arrestin-1-induced NF-kB activation is mediated by the AKT pathway as shown by IL-1 beta-stimulated chondrocytes treated with AKT inhibitor. Finally, a specific HA-blocking peptide (Pep-1) has confirmed the inflammatory role of degraded HA as a mediator of the IL-1 beta-induced activation of beta-arrestin-1.
机译：Beta-arrestin-1（beta-arrestin-1）是一种衔接蛋白，在G蛋白激活的终止中起作用，似乎参与了炎症反应的介导。白介素-1 beta（IL-1 beta）通过涉及透明质酸（HA）降解的机制引起炎症介质的表达，从而促进了Toll-like受体4（TLR-4）和CD44的激活。两种受体的刺激均可诱导核因子κB（NF-kB）激活，该因子通过转化生长因子激活的激酶-1（TAK-1）进而刺激转录的炎症介质。由于β-arrestin-1在关节炎中起炎症作用，因此我们研究了β-arrestin-1在小鼠软骨细胞中IL-1β诱导的炎症反应模型中的作用。 IL-1β治疗可显着增加软骨细胞TLR-4，CD44，β-arrestin-1，TAK-1和丝氨酸/苏氨酸激酶（AKT）mRNA表达及相关蛋白水平。 NF-kB也被随后的肿瘤坏死因子-α，白介素-6和诱导型一氧化氮合酶上调显着激活。用β-arrestin-1和/或AKT和/或TAK-1特异性抑制剂治疗IL-1β刺激的软骨细胞可显着降低所有参数，尽管TAK-1介导的途径所产生的抑制作用比β-arrestin-1。 β-Arrestin-1诱导的NF-kB激活是由AKT途径介导的，如用AKT抑制剂治疗的IL-1β刺激的软骨细胞所示。最后，一种特定的HA阻断肽（Pep-1）已确认降解的HA作为IL-1β诱导的β-arrestin-1活化的介质的炎症作用。

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