Identification of a specific transporter on extracellular release of ATP

细胞外释放 ATP 的特定转运蛋白的鉴定

基本信息

批准号：
17590234
负责人：
KATSURAGI Takeshi
金额：
$ 2.3万
依托单位：
Fukuoka University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2005
资助国家：
日本
起止时间：
2005 至 2006
项目状态：
已结题

项目摘要

In recent years, ATP is well-known to be served as a modulator of cellular functions via P2X and P2Y purinoceptors. However, so far, the mechanisms underlying the extracellular release of ATP and the related Ca^<2+>-signaling. remains unclear. The present subject was undertaken to clarify these points. The studies consist of separate parts as follows. First, in the study with cultured T. coli cells, bradykinin elicited ATP release mediated by B2 receptors, then, increased Ins(1,4,5)P3 production, triggering Ca^<2+>-release from endoplasmic reticulum. The Ca^<2+>-signal attains to the cell membrane and then, the membrane transporter, MRP1, will be activated. Finally, ATP is exported by MRP1 transporter. CFTR transporter and hemi channels were not involved in the export of ATP evoked by bradykinin.In another study, it has been evaluated whether some Ca^<2+>-signaling contributes to the release of ATP evoked by bradykinin from cultured vas deferens smooth muscle cells. Bradykinin via RyR2 receptor elicits an increase of Ca^<2+> release from ER. The Ca^<2+> signaling was transferred to mitochondria (Mt) and, then, the elevation of Ca^<2+> levels in Mt activates the Ca^<2+>-dependent dehydrogenases and further the electron transfer system resulting in the enhancement of ATP synthesis in Mt. Finally, the ATP signals attain the cell membrane and the membranous ATP transport system is promoted. In conclusion, these findings suggest that the ATP export is triggered by the characteristic Ca^<2+> signaling from ER to MT.

近年来，ATP众所周知，可以通过P2X和P2Y Purinoceptors作为细胞功能的调节剂。但是，到目前为止，ATP的细胞外释放和相关的CA^<2+>信号传导的机制。仍然不清楚。目前的主题是为了澄清这些观点。这些研究包括单独的部分，如下所示。首先，在用培养的肠杆菌细胞的研究中，缓激肽引起了由B2受体介导的ATP释放，然后增加了INS（1,4,5）P3的产生，从而触发了Ca^<2+> - 从内质网释放。 CA^<2+> - 信号将获得细胞膜，然后将膜转运蛋白MRP1激活。最后，ATP由MRP1转运蛋白导出。 CFTR转运蛋白和Hemi通道没有参与Bradykinin引起的ATP的导出。在另一项研究中，已经评估了某些CA^<2+> - 信号是否有助于培养的VAS deferens平滑肌细胞从培养的Vas deferens Smoolcle Smoole Smolecle Smolescle Smolescle Smoless Smootle Smuscle Smuscle Smuscle Smulake of Specoke的ATP。 Bradykinin通过RYR2受体引起的Ca^<2+>从ER释放。 The Ca^<2+> signaling was transferred to mitochondria (Mt) and, then, the elevation of Ca^<2+> levels in Mt activates the Ca^<2+>-dependent dehydrogenases and further the electron transfer system resulting in the enhancement of ATP synthesis in Mt. Finally, the ATP signals attain the cell membrane and the membranous ATP transport system is promoted.总之，这些发现表明ATP导出是由从ER到MT的特征Ca^<2+>触发的。

项目成果

期刊论文数量（24）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Vascular Na^+/Ca^<2+> exchanger : implications for the pathogenesis and therapy of salt-dependent hypertention.

血管Na^/Ca^2交换器：对盐依赖性高血压的发病机制和治疗的影响。

DOI：
发表时间：
2006
期刊：
Am. J. Physiol. 290(3)
影响因子：
0
作者：
Suzuki H;Momoi N;Ono T;Maeda S;Shikama Y;Matsuoka I;Suzuki H;Kimura J.;中谷晴昭;T.Iwamoto
通讯作者：
T.Iwamoto

Contribution of anaphylatoxins to allergic inflammation in human lungs

过敏毒素对人类肺部过敏性炎症的影响