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首页> 外文期刊>Journal of Cellular Physiology >Low Shear Stress Attenuates COX-2 Expression Induced by Resistin in Human Osteoarthritic Chondrocytes
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Low Shear Stress Attenuates COX-2 Expression Induced by Resistin in Human Osteoarthritic Chondrocytes

机译：低剪切应力变弱cox - 2的表达抵抗素在人类引起的骨关节炎的软骨细胞

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Low shear stress has been proposed to play a reparative role in modulating cartilage homeostasis. Recently, epidemiological studies have found a positive correlation between the resistin level in serum and synovial fluid and osteoarthritis (OA) severity in patients. However, the effect of moderate shear stress on the catabolic stimulation of resistin in OA chondrocytes remains unclear. Hence, this study was to investigate whether low shear stress could regulate resistin-induced catabolic cyclooxygenase (COX)-2 expression in human OA chondrocytes and the underlying mechanism. Human OA chondrocytes and SW1353 chondrosarcoma cells were used in this study. Two modes of low shear stress (2 dyn/cm(2)), pre-shear and post-shear, were applied to the chondrocytes. A specific activator and siRNAs were used to investigate the mechanism of low shear stress-regulated COX-2 expression of resistin induction. We found that human OA chondrocytes exposed to different modes of low shear stress elicit an opposite effect on resistin-induced COX-2 expression: pre-shear for a short duration attenuates the resistin effect by inhibiting the transcription factor nuclear factor (NF)-kappa B- p65 subunit and the cAMP response element binding protein; however, post-shear over a longer duration enhances the resistin effect by activating only the NF kappa B- p65 subunit. Moreover, our results demonstrated that the regulation of both shear modes in resistin-stimulated COX-2 expression occurs through increasing AMP-activated protein kinase activation and then sirtuin 1 expression. This study elucidates the detailed mechanism of low shear stress regulating the resistin-induced catabolic COX-2 expression and indicates a possible reparative role of moderate shear force in resistin-stimulated OA development.
机译：低剪切应力提出了发挥在调节软骨修复的作用体内平衡。发现之间的正相关关系血清抵抗素水平和滑液骨关节炎(OA)患者的严重程度。然而,温和的剪切应力的影响抵抗素在OA的异化的刺激软骨细胞仍不清楚。是调查低剪切应力是否可以调节resistin-induced分解环氧合酶(COX) 2表达在人类OA软骨细胞和底层机制。OA软骨细胞和SW1353软骨肉瘤细胞被用于这项研究。压力(2(2)达因/厘米),pre-shear post-shear,被应用于软骨细胞。激活剂和siRNAs被用于调查低剪切stress-regulated cox - 2的机制抵抗素的表达归纳。人类OA软骨细胞暴露于不同的模式低剪切应力引起一个相反的效果resistin-induced cox - 2表达:pre-shear短时间内变弱抵抗素的效果通过抑制转录因子核因子(NF)κB - p65单元和营地反应元件结合蛋白;post-shear长持续时间提高了通过激活只有NF卡帕抵抗素的影响B - p65亚基。表明,剪切的规定在resistin-stimulated cox - 2的表达模式通过增加活化蛋白发生激酶激活然后sirtuin蛋白1表达。本研究论述了详细的机制低剪切应力调节resistin-induced分解代谢的cox - 2表达和表示可能的修复作用温和的剪切力在resistin-stimulated办公自动化的发展。

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