Purinergic Signal. 2010 Dec;6(4):383-91. doi: 10.1007/s11302-010-9203-x. Epub 2010 Nov 3.
Nucleoside di- and triphosphates and adenosine regulate several components of the mucocilairy clearance process (MCC) that protects the lung against infections, via activation of epithelial purinergic receptors. However, assessing the contribution of individual nucleotides to MCC functions remains difficult due to the complexity of the mechanisms of nucleotide release and metabolism. Enzymatic activities involved in the metabolism of extracellular nucleotides include ecto-ATPases and secreted nucleoside diphosphokinase (NDPK) and adenyl kinase, but potent and selective inhibitors of these activities are sparse. In the present study, we discovered that ebselen markedly reduced NDPK activity while having negligible effect on ecto-ATPase and adenyl kinase activities. Addition of radiotracer [γ(32)P]ATP to human bronchial epithelial (HBE) cells resulted in rapid and robust accumulation of [(32)P]-inorganic phosphate ((32)Pi). Inclusion of UDP in the incubation medium resulted in conversion of [γ(32)P]ATP to [(32)P]UTP, while inclusion of AMP resulted in conversion of [γ(32)P]ATP to [(32)P]ADP. Ebselen markedly reduced [(32)P]UTP formation but displayed negligible effect on (32)Pi or [(32)P]ADP accumulations. Incubation of HBE cells with unlabeled UTP and ADP resulted in robust ebselen-sensitive formation of ATP (IC(50) = 6.9 ± 2 μM). This NDPK activity was largely recovered in HBE cell secretions and supernatants from lung epithelial A549 cells. Kinetic analysis of NDPK activity indicated that ebselen reduced the V(max) of the reaction (K(i) = 7.6 ± 3 μM), having negligible effect on K(M) values. Our study demonstrates that ebselen is a potent non-competitive inhibitor of extracellular NDPK.
核苷二磷酸和三磷酸以及腺苷通过激活上皮嘌呤能受体调节粘液纤毛清除过程 (MCC) 的几个组成部分,该过程可保护肺部免受感染。然而,由于核苷酸释放和代谢机制的复杂性,评估单个核苷酸对 MCC 功能的贡献仍然很困难。参与细胞外核苷酸代谢的酶活性包括外核苷酸酶和分泌核苷二磷酸激酶 (NDPK) 和腺嘌呤激酶,但这些活性的有效且选择性抑制剂却很少。在本研究中,我们发现依布硒啉可显着降低 NDPK 活性,而对外核苷酸酶和腺嘌呤激酶活性的影响可忽略不计。将放射性示踪剂 [γ(32)P]ATP 添加到人支气管上皮 (HBE) 细胞中会导致 [(32)P]-无机磷酸盐 ((32)Pi) 的快速和强烈积累。在孵育培养基中加入 UDP 会导致 [γ(32)P]ATP 转化为 [(32)P]UTP,而加入 AMP 会导致 [γ(32)P]ATP 转化为 [(32)P]ADP。依布硒啉显着减少 [(32)P]UTP 的形成,但对 (32)Pi 或 [(32)P]ADP 的积累几乎没有影响。用未标记的 UTP 和 ADP 孵育 HBE 细胞会导致 ATP 的依布硒啉敏感形成(IC(50) = 6.9 ± 2 μM)。这种 NDPK 活性在 HBE 细胞分泌物和肺上皮 A549 细胞的上清液中得到了很大的恢复。NDPK 活性的动力学分析表明,依布硒啉降低了反应的 V(max)(K(i) = 7.6 ± 3 μM),对 K(M) 值几乎没有影响。我们的研究表明,依布硒啉是细胞外 NDPK 的有效非竞争性抑制剂。