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首页> 外文期刊>Journal of Cellular Physiology >24R,25-(OH)(2)D(3) mediates its membrane receptor-dependent effects on protein kinase C and alkaline phosphatase via phospholipase A(2) and cyclooxygenase-1 but not cyclooxygenase-2 in growth plate chondrocytes.
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24R,25-(OH)(2)D(3) mediates its membrane receptor-dependent effects on protein kinase C and alkaline phosphatase via phospholipase A(2) and cyclooxygenase-1 but not cyclooxygenase-2 in growth plate chondrocytes.

机译：24 r, 25 (OH) D(2)(3)介导的膜receptor-dependent对蛋白激酶C的影响通过磷脂酶和碱性磷酸酶(2)和cyclooxygenase-1但不是cyclooxygenase-2生长板软骨细胞。

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Recent studies have shown that 24R,25-(OH)(2)D(3) mediates its effects on growth plate chondrocytes via membrane receptors. This study examined the roles of phospholipase A(2) (PLA(2)) and cyclooxygenase (Cox) in the mechanism of action of 24R, 25-(OH)(2)D(3) in resting zone chondrocytes in order to determine whether the activity of one or both enzymes provides a regulatory checkpoint in the signaling pathway resulting in increased protein kinase C (PKC) activity. We also determined whether constitutive or inducible Cox is involved. Cultures were incubated with 24R, 25-(OH)(2)D(3) for 90 min to measure PKC or for 24 h to measure physiological responses ([(3)H]-thymidine incorporation, alkaline phosphatase-specific activity, [(35)S]-sulfate incorporation). Based on RT-PCR and Northern blot analysis, resting zone chondrocytes express mRNAs for both Cox-1 and Cox-2. Levels of mRNA for both proteins were unchanged from control levels after a 24-h incubation with 24R,25-(OH)(2)D(3). To examine the role of Cox, the cultures were also treated with resveratrol (a specific inhibitor of Cox-1), NS-398 (a specific inhibitor of Cox-2), or indomethacin (a general Cox inhibitor). Cox-1 inhibition resulted in effects on proliferation, differentiation, and matrix production typical of 24R, 25-(OH)(2)D(3). In contrast, inhibition of Cox-2 had no effect, indicating that 24R,25-(OH)(2)D(3) exerts its effects via Cox-1. Inhibition of Cox-1 also blocked 24R,25-(OH)(2)D(3)-dependent increases in PKC. Activation of PLA(2) with melittin inhibited 24R, 25-(OH)(2)D(3)-dependent stimulation of PKC, and inhibition of PLA(2) with quinacrine stimulated PKC in response to 24R, 25-(OH)(2)D(3). Inclusion of resveratrol reduced the melittin-dependent inhibition of PLA(2) and caused an increase in quinacrine-stimulated PLA(2) activity. Metabolism of arachidonic acid to leukotrienes is not involved in the response to 24R, 25-(OH)(2)D(3) because inhibition of lipoxygenase had no effect. The effect of 24R,25-(OH)(2)D(3) was specific because 24S,25-(OH)(2)D(3), the biologically inactive stereoisomer, failed to elicit a response from the cells. These results support the hypothesis that 24R, 25-(OH)(2)D(3) exerts its effects via more than one signaling pathway and that these pathways are interrelated via the modulation of PLA(2). PKC regulation may occur at multiple stages in the signal transduction cascade. Copyright 2000 Wiley-Liss, Inc.
机译：最近的研究表明,r, 24日25 - D (OH) (2) (3)介导对生长板软骨细胞的影响通过膜受体。角色的磷脂酶(2)和(解放军(2))环氧合酶(Cox)的作用机制24 r, 25 (OH) D(2)(3)在休息区域软骨细胞以确定提供了一个或两个酶的活性在信号通路管理检查点导致增加蛋白激酶C (PKC)活动。考克斯或诱导。孵化24 r, 25 - D (OH)(2)(3)为90分钟测量PKC或24小时测量生理反应([(3)H]胸腺嘧啶核苷掺入,碱性phosphatase-specific活动,[(35) S]硫酸公司)。和北部污点分析、休息区域软骨细胞表达mrna Cox-1和cox - 2。24小时后从控制水平不变孵化24 r, 25 - (OH)(2)(3)。考克斯的作用,文化也治疗白藜芦醇(Cox-1特定抑制剂),ns - 398(特定的cox - 2抑制剂),或吲哚美辛(一般Cox抑制剂)。抑制导致对扩散的影响,分化,矩阵生产的典型24 r, 25 (OH) D(2)(3)。cox - 2没有效果,表明24 r, 25 (OH) D(2)(3)通过Cox-1施加其影响。抑制Cox-1也屏蔽了24 r, 25 (OH) D(2)(3)端依赖增加PKC。激活的解放军(2)蜂毒肽抑制24 r,25 (OH) D(2)(3)端依赖刺激的PKC和奎纳克林刺激抑制解放军(2)PKC在回应24 r, 25 - (OH)(2)(3)。白藜芦醇的减少了melittin-dependent解放军(2)和抑制的增加引起的quinacrine-stimulated解放军(2)活动。花生四烯酸的白细胞三烯不是参与反应的24 r, 25 - D (OH) (2) (3)因为抑制脂肪氧合酶没有效果。24 r的影响,25 (OH) D(2)(3)是特定的因为24 s, 25 - (OH)(2)(3),生物不活跃的立体异构体,未能引起细胞的响应。假设24 r, 25 (OH) D(2)(3)产生通过多个信号通路的影响通过的,这些途径都是相互关联的解放军(2)的调制。信号转导的多个阶段级联。

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