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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Interleukin 1β suppresses transforming growth factor-induced inorganic pyrophosphate (PP_i) production and expression of the PP_i-generating enzyme PC-1 in human chondrocytes
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Interleukin 1β suppresses transforming growth factor-induced inorganic pyrophosphate (PP_i) production and expression of the PP_i-generating enzyme PC-1 in human chondrocytes

机译：白介素1β抑制人软骨细胞中转化生长因子诱导的无机焦磷酸盐（PP_i）的产生和PP_i生成酶PC-1的表达

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摘要

Articular cartilage chondrocytes have the unique ability to elaborate large amounts of extracellular pyrophosphate (PP_i), and transforming growth factor β (TGFβ) appears singular among cartilage regulatory factors in stimulating PP_i production. TGFβ caused a time and dose-dependent increase in intracellular and extracellular PP_i in human articular chondrocyte cultures. TGFβ and interleukin 1β (IL-1β) antagonistically regulate certain chondrocyte functions. IL-1β profoundly inhibited basal and TGFβ-induced PP_i elaboration. To address mechanisms involved with the regulation of PP_i synthesis by IL-1β and TGFβ, we analyzed the activity of the PP_i-generating enzyme NTP py-rophosphohydrolase (NTPPPH) and the PP_i-hydrolyzing enzyme alkaline phosphatase. Human chondrocyte NTPPPH activity was largely attributable to plasma cell membrane glycoprotein 1, PC-1. Furthermore, TGFβ induced comparable increases in the activity of extracellular PP_i, intracellular PP_i, and cellular NTPPPH and in the levels of PC-1 protein and mRNA in chondrocytes as well as a decrease in alkaline phosphatase. All of these TGFβ-induced responses were completely blocked by IL-1β. Thus, IL-1β may be an important regulator of mineralization in chondrocytes by inhibiting TGFβ-induced PP_i production and PC-1 expression.
机译：关节软骨软骨细胞具有形成大量细胞外焦磷酸盐（PP_i）的独特能力，并且在刺激PP_i产生的软骨调节因子中，转化生长因子β（TGFβ）显得很奇异。 TGFβ导致人关节软骨细胞培养物中细胞内和细胞外PP_i的时间和剂量依赖性增加。 TGFβ和白介素1β（IL-1β）拮抗某些软骨细胞的功能。 IL-1β显着抑制基础和TGFβ诱导的PP_i形成。为了解决由IL-1β和TGFβ调控PP_i合成的机制，我们分析了产生PP_i的酶NTP焦磷酸水解酶（NTPPPH）和水解PP_i的碱性磷酸酶的活性。人软骨细胞NTPPPH活性主要归因于浆细胞膜糖蛋白1，PC-1。此外，TGFβ诱导软骨细胞中胞外PP_i，胞内PP_i和细胞NTPPPH的活性和PC-1蛋白和mRNA的水平相当的增加，以及碱性磷酸酶的减少。所有这些TGFβ诱导的反应均被IL-1β完全阻断。因此，IL-1β通过抑制TGFβ诱导的PP_i产生和PC-1表达，可能是软骨细胞矿化的重要调节剂。

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