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首页> 外文期刊>Journal of Cellular Physiology >Hypoxia stimulates vesicular ATP release from rat osteoblasts.
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Hypoxia stimulates vesicular ATP release from rat osteoblasts.

机译：从大鼠缺氧刺激水泡ATP释放造骨细胞。

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Many neuronal and non-neuronal cell types release ATP in a controlled manner. After release, extracellular ATP (or, following hydrolysis, ADP) acts on cells in a paracrine manner via P2 receptors. Extracellular nucleotides are now thought to play an important role in the regulation of bone cell function. ATP (and ADP), acting via the P2Y(1) receptor, stimulate osteoclast formation and activity, whilst P2Y(2) receptor stimulation by ATP (or UTP) inhibits bone mineralization by osteoblasts. We found that rat calvarial osteoblasts released ATP constitutively, in a differentiation-dependent manner, with mature, bone-forming osteoblasts releasing up to sevenfold more ATP than undifferentiated, proliferating cells. The inhibitors of vesicular exocytosis, monensin, and N-ethylmaleimide (1-1,000 microM) inhibited basal ATP release by up to 99%. The presence of granular ATP-filled vesicles within the osteoblast cytoplasm was demonstrated by quinacrine staining. Exposure to hypoxia (2% O(2)) for up to 3 min increased ATP release from osteoblasts up to 2.5-fold without affecting cell viability. Peak concentrations of ATP released into culture medium were >1 microM, which equates with concentrations known to exert significant effects on osteoblast and osteoclast function. Monensin and N-ethylmaleimide (100 microM) attenuated the hypoxia-induced ATP release by up to 80%. Depletion of quinacrine-stained vesicles was also apparent after hypoxic stimulation, indicating that ATP release had taken place. These data suggest that vesicular exocytosis is a key mediator of ATP release from osteoblasts, in biologically significant amounts. Moreover, increased extracellular ATP levels following acute exposure to low O(2) could influence local purinergic signaling and affect the balance between bone formation and bone resorption.
机译：许多神经元和non-neuronal细胞释放ATP控制的方式。细胞外ATP(或者水解后,ADP)以旁分泌的方式作用于细胞通过P2受体。认为中发挥重要作用调节骨细胞的功能。代理通过P2Y受体(1),刺激破骨细胞形成和活动,同时P2Y (2)通过ATP (UTP)抑制受体刺激由成骨细胞骨矿化。大鼠颅盖的成骨细胞释放ATP结构上,differentiation-dependent方式,与成熟,成骨造骨细胞释放ATP 7倍比未分化,增殖细胞。抑制剂的水泡胞外分泌、莫能菌素和N-ethylmaleimide (1 - 1000 microM)抑制基底ATP释放高达99%。粒状ATP-filled囊泡内成骨细胞细胞质被证明了奎纳克林染色。O(2)) 3分钟增加ATP释放2.5倍而不影响细胞成骨细胞生存能力。到培养基microM > 1,与已知浓度产生显著对成骨细胞和破骨细胞功能的影响。莫能菌素和N-ethylmaleimide (100 microM)减毒诱导ATP释放到80%。也明显缺氧刺激后,表明ATP释放。这些数据表明,水泡胞外分泌ATP释放成骨细胞的关键中介,生物大量。增加细胞外ATP水平以下急性暴露于低O(2)可能会影响当地的purinergic信号和影响平衡骨形成和骨吸收之间的关系。

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