Oxygen-glucose deprivation induces ATP release via maxi-anion channels in astrocytes.
Oxygen-glucose deprivation induces ATP release via maxi-anion channels in astrocytes.
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DOI：
10.1007/s11302-007-9077-8
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发表时间：
2008-06
影响因子：
3.5
通讯作者：
Okada, Yasunobu
中科院分区：
文献类型：
--
作者：
Liu, Hong-Tao;Sabirov, Ravshan Z.;Okada, Yasunobu
三磷酸腺苷是一种主要的胶质递质，是神经胶质细胞和神经细胞之间相互作用的信号分子。已有研究表明，在非缺血条件下，星形胶质细胞会对多种刺激做出反应，从而释放出ATP。在这项研究中，使用荧光素-荧光素酶分析，我们发现在原代培养的小鼠星形胶质细胞也表现出大量的ATP释放，以响应模拟的缺氧-葡萄糖剥夺(OGD)的缺血应激。Gd~(3+)和花生四烯酸可抑制OGD诱导的ATP释放，但容量敏感的外向整流性Cl-−通道阻断剂、囊性纤维化跨膜电导调节剂、多药耐药相关蛋白、连接蛋白或膜联蛋白半通道、P2X7受体和胞外囊泡运输阻断剂均不能抑制OGD诱导的ATP释放。在单个星形胶质细胞的贴壁贴片中，OGD引起对Gd3+和花生四烯酸敏感的最大阴离子通道的激活。该通道对−具有渗透性，渗透率为PATP0.11/Pcl = 。因此，缺血应激可诱导星形胶质细胞释放ATP，最大阴离子通道可能是缺血条件下的主要ATP释放途径。
ATP represents a major gliotransmitter that serves as a signaling molecule for the cross talk between glial and neuronal cells. ATP has been shown to be released by astrocytes in response to a number of stimuli under nonischemic conditions. In this study, using a luciferin-luciferase assay, we found that mouse astrocytes in primary culture also exhibit massive release of ATP in response to ischemic stress mimicked by oxygen-glucose deprivation (OGD). Using a biosensor technique, the local ATP concentration at the surface of single astrocytes was found to increase to around 4 μM. The OGD-induced ATP release was inhibited by Gd3+ and arachidonic acid but not by blockers of volume-sensitive outwardly rectifying Cl− channels, cystic fibrosis transmembrane conductance regulator (CFTR), multidrug resistance-related protein (MRP), connexin or pannexin hemichannels, P2X7 receptors, and exocytotic vesicular transport. In cell-attached patches on single astrocytes, OGD caused activation of maxi-anion channels that were sensitive to Gd3+ and arachidonic acid. The channel was found to be permeable to ATP4− with a permeability ratio of PATP/PCl = 0.11. Thus, it is concluded that ischemic stress induces ATP release from astrocytes and that the maxi-anion channel may serve as a major ATP-releasing pathway under ischemic conditions.
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ATP通过阴离子通道释放。
影响因子：
3.5
作者：
Sabirov, Ravshan Z;Okada, Yasunobu
通讯作者：
Okada, Yasunobu
影响因子：
6.2
作者：
Shinozaki, Y;Koizumi, S;Inoue, K
通讯作者：
Inoue, K
DOI：
10.1073/pnas.95.26.15735
发表时间：
1998-12-22
影响因子：
11.1
作者：
Cotrina, ML;Lin, JHC;Nedergaard, M
通讯作者：
Nedergaard, M
DOI：
10.1085/jgp.118.3.251
发表时间：
2001-09
期刊：
The Journal of general physiology
影响因子：
--
作者：
Sabirov RZ;Dutta AK;Okada Y
通讯作者：
Okada Y
影响因子：
4.8
作者：
Coco, S;Calegari, F;Verderio, C
通讯作者：
Verderio, C