Maxi-anion channel as a candidate pathway for osmosensitive ATP release from mouse astrocytes in primary culture
Maxi-anion channel as a candidate pathway for osmosensitive ATP release from mouse astrocytes in primary culture
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DOI：
10.1038/cr.2008.49
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发表时间：
2008-05-01
期刊：
影响因子：
44.1
通讯作者：
Okada, Yasunobu
中科院分区：
文献类型：
--
作者：
Liu, Hong-Tao;Toychiev, Abduqodir H.;Okada, Yasunobu
在本研究中，我们的目的是评估的途径，有助于从小鼠星形胶质细胞在低渗应激的ATP释放。我们首先研究了过去几年来提出的可能构成ATP释放途径的蛋白质的mRNA表达。在使用对照和肿胀星形胶质细胞的RT-PCR分析中，观察到连接蛋白（Cx 32、Cx 37、Cx43）、泛连接蛋白1（Px 1）、P2 X7受体、MRP 1和MDR 1的预期大小的cDNA片段扩增，但未观察到CFTR。胞吐囊泡释放、间隙连接半通道、CFTR、MRP 1、MDR 1、P2 X7受体和体积敏感性外向整流氯离子通道的抑制剂对星形胶质细胞的大量ATP释放没有显著影响。相比之下，低渗诱导的ATP释放星形胶质细胞是最有效地抑制钆（50 μ M），抑制剂的最大阴离子通道，最近已被证明是作为一个途径，从其他几种细胞类型的ATP释放。因此，我们建议，最大阴离子通道构成了肿胀诱导的ATP释放培养的小鼠星形胶质细胞以及一个主要途径。
In the present study, we aimed to evaluate the pathways contributing to ATP release from mouse astrocytes during hypoosmotic stress. We first examined the expression of mRNAs for proteins constituting possible ATP-releasing pathways that have been suggested over the past several years. In RT-PCR analysis using both control and osmotically swollen astrocytes, amplification of cDNA fragments of expected size was seen for connexins (Cx32, Cx37, Cx43), pannexin 1 (Px1), the P2X7 receptor, MRP1 and MDR1, but not CFTR. Inhibitors of exocytotic vesicular release, gap junction hemi-channels, CFTR, MRP1, MDR1, the P2X7 receptor, and volume-sensitive outwardly rectifying chloride channels had no significant effects on the massive ATP release from astrocytes. In contrast, the hypotonicity-induced ATP release from astrocytes was most effectively inhibited by gadolinium (50 mu M), an inhibitor of the maxi-anion channel, which has recently been shown to serve as a pathway for ATP release from several other cell types. Thus, we propose that the maxi-anion channel constitutes a major pathway for swelling-induced ATP release from cultured mouse astrocytes as well.